The Stanford Alzheimer’s Disease Research Center (ADRC) supports internal research in the form of developmental projects and Research Education Component (REC) fellowships. Developmental projects are usually conducted over a two year period and are funded for up to $250,000 each. The ADRC has selected four projects (two in 2020 and two in 2021), and we anticipate new projects in 2022 and 2023. Developmental project grants are intended for junior faculty level investigators and for more senior investigators whose research lies in other areas and who now want to work in the field of Alzheimer disease and related disorders.
The Stanford ADRC contributes de-identified data and biological resources to registries and repositories supported by the National Institute on Aging. It supports other research at Stanford University and at other institutions. Center support can include de-identified data (clinical, neuropsychological, structural and molecular brain imaging, genetic, ‘omics, microbiome, and neuropathological), fluid biospecimens obtained from ADRC volunteers (plasma, CSF), fibroblast cell lines, autopsy tissues, biostatistical consultation, and research guidance.
The Stanford ADRC supports research training and education in a variety of ways. The REC fellowship program is described more fully below. This program provides integrated clinical and basic science training opportunities and mentored research experiences. It is designed to prepare the next generation of researchers for careers in brain aging and in Alzheimer’s disease and related disorders.
Tabs below provide additional information on developmental projects, REC fellowship projects, ADRC publications, and application materials for both developmental projects and REC fellowships. Titles of internal research supported by the Stanford ADRC during the 2015–2019 funding period are also shown.
JEDI Developmental Project (2023) 1:
Principal investigator: Michelle Lin, MD, MPH, MS, Associate Professor of Medicine
Title: Improving Access to Geriatric Emergency Care among Older Adults with Dementia
Project description: Older adults and persons living with dementia (PLWD) account for a growing share of U.S. Emergency Department visits. They are more likely to be hospitalized and to experience adverse events associated with hospitalization, including iatrogenic harm, functional decline, and readmissions. Geriatric Emergency Departments (GEDs) have emerged as a promising model of care for older adults and PLWD. However, little is known about disparities in access to GEDs and their adoption among hospitals serving historically marginalized groups. This project aims to address this knowledge gap by (1) measuring disparities in access to GEDs among PLWD, including differences by race, ethnicity, income, and geographic location and (2) identifying barriers and facilitators to the adoption of GEDs in safety-net hospitals serving PLWD. These findings will inform policy and practice recommendations to improve access to GEDs for PLWD and serve as preliminary data for an R01 to promote equity in the adoption of GEDs and reduce disparities for PLWD from historically marginalized groups.
JEDI Developmental Project (2023) 2:
Principal investigator: Holly Tabor, PhD, Associate Professor of Medicine, Stanford University
Title: IDD-TRANSFORM: Building an Engaged and Diverse Community-Based Cohort for Aging, Alzheimer’s, and Down’s Syndrome
Project description: While the importance of Alzheimer’s to overall public health has been long recognized, the etiology and challenges of Alzheimer’s in patients with Down Syndrome (DS) has been less studied or well characterized. In recent years, the high prevalence of Alzheimer’s disease in patients with DS, as well as the earlier age of onset, has led researchers to increase their interest and focus on studies of the disease in this population. However, such studies lack data about the specific etiology, characteristics, lived experiences, and health and healthcare access challenges of adults with DS in general, and most specifically aging adults with DS. It is imperative to engage with adults with DS and their caregivers themselves, in order to characterize their lived experience and understand the issues driving disparities in health outcomes and health care access. This direct engagement can help facilitate the development of interventions that are likely to improve health outcomes, health access, and quality of life for this population. The goal of our grant is to build an engaged and diverse community-based cohort to study AD and DS, and it has four aims to : 1) to create a Core Advisory Board of researchers, health care workers, adults with Down’s Syndrome (DS), DS caregivers, and community agencies/partners, to collaboratively design and implement a Community Based Participatory Research (CBPR) approach to studying Alzheimer’s and DS in a racially, ethnically, and socio-economically diverse population in the Bay Area; 2) To develop language- and culturally- concordant educational flyers and Virtual Health Forum sessions about DS and Alzheimer’s disease; 3) To characterize knowledge, needs, and lived experiences of DS adults with Alzheimer’s Disease, by conducting focus groups and interviews with adults with DS, caregivers of adults with DS, and community agencies/partners that serve adults with DS/IDD; and 4) Develop a research proposal to submit to NIH in Fall 2025 on DS and AD in diverse populations.
Developmental Project (2023) 4.1:
Principal investigator: Helen Bronte-Stewart MD MSE, FAAN, FANA, John E. Cahill Family Professor, Director, Human Motor Control and Neuromodulation Lab (HCMNL), Co-Director, Stanford Balance Center, Department of Neurology and Neurological Sciences, Department of Neurosurgery (by courtesy), Stanford University School of Medicine
Title: Characterizing cholinergic deficits and their impact on cognitive-motor deficits across progressive neurodegenerative diseases
Project description: There is a critical unmet need for effective treatments to stabilize cognitive decline in progressive neurodegenerative diseases such as Parkinson’s disease, Dementia with Lewy Bodies, and Alzheimer’s disease. Despite varying pathologies, these diseases share decline in a common brain network, known as the cortical cholinergic network, which is responsible for cognitive functions such as arousal, attention, information processing, and aspects of memory. This degeneration begins early in the disease, often before these cognitive deficits can be identified. This presents a major challenge, as by the time of diagnosis, the severity of this decline makes it difficult to successfully intervene. However, there is an increasing amount of literature supporting the idea that there may be motor components of cognitive impairment that manifest themselves significantly earlier, termed the cognitive-motor syndrome. These higher resolution behaviors offer an opportunity to identify cognitive-related deficits earlier when interventions may be more effective and allow tracking of response to therapies over time. We aim to investigate the relationships between this shared degeneration and measures of cognitive-motor syndrome in people with Parkinson’s disease, Dementia with Lewy Bodies, and Alzheimer’s disease using multi-modal brain imaging techniques. The outcome of this research will provide unique insight into the underlying neurobiology of cognitive-motor deficits of each disease.
Developmental Project (2023) 4.2
Principal investigator: Julia Kaltschmidt, PhD, Associate Professor of Neurosurgery, Stanford Neurosciences Institute Faculty Scholar, Firmenich Next Generation Faculty Scholar, Stanford University School of Medicine
Title: Enteric pathophysiology in Parkinson’s disease
Project description: Parkinson’s Disease (PD) is a progressive, age-related movement disorder that affects more than 5 million people worldwide. There is currently no effective tool for diagnosing PD before movement symptoms manifest. While primarily characterized as a movement disorder, non-motor PD symptoms, such as constipation, have been identified to precede motor symptoms by years. The characteristic sign of PD in the brain are aggregations of α-synuclein protein. However, accumulating evidence suggests that α-synuclein aggregations begin in and migrate from gut (enteric) neurons. Enteric α-synuclein aggregates, proposed to be triggered in part by environmental risk factors, such as herbicide exposure, are thus attractive as a potential early biological marker for diagnosis of PD. We will study the initial stages of PD using two mouse models of α-synuclein aggregation: 1) exposure to the herbicide paraquat, and 2) viral overexpression of human α-synuclein in the mouse gut. Using these models, we aim to identify cells in the gut most susceptible to α-synuclein aggregation and to trace neuronal pathways through which α-synuclein may migrate from the gut to the brain, providing information essential to understanding the pathophysiology of early PD.
Developmental Project (2023) 4.3
Principal investigator: Brad Zuchero, PhD, Assistant Professor of Neurosurgery, Stanford University School of Medicine
Title: Myelin dysfunction in Alzheimer's disease
Project description: Myelin is essential in the central nervous system (CNS) for rapid nerve signaling and neuroprotection. CNS myelin is built by oligodendrocytes, specialized glial cells that undergo dramatic cell biology changes to form and maintain myelin. Myelin dysfunction is emerging as central to Alzheimer’s disease (AD), yet the precise contributions of myelin to AD remain largely unexplored. Several recent studies using single-cell transcriptomics of human AD patients or mouse models of AD have consistently revealed that myelin and oligodendrocyte dysfunction occurs early in AD. A major knowledge gap is the extent to which myelin dysfunction contributes to neurodegeneration and cognitive decline, and what cellar mechanisms are responsible for this. To address these questions, we will start a new project leveraging our expertise in myelin cell biology together with the resources and expertise of the ADRC. We will test the oligodendrocyte-autonomous roles of several AD-linked genes to determine whether they are sufficient to perturb oligodendrocyte differentiation, myelination, and/or myelin integrity. Overall, the goal of this proposal is to launch a new AD-focused research direction—bringing our expertise in myelin cell biology to the question of how myelin dysfunction contributes to AD. Successful completion of this project would provide important insights into myelin’s role in neurodegeneration and may reveal new therapeutic avenues for preserving or recovering cognitive function in AD.
Developmental research project (2022) 3.1
Principal investigator: Michael Belloy, PhD, Instructor, Department of Neurology
Title: Disentangling sex-specific risk for Alzheimer's disease through state-of-the-art genomics.
Project description: Alzheimer’s disease has a very strong genetic component, with heritability estimates of this disorder being more than 50%. It is further clear that men and women develop Alzheimer’s disease disproportionally and that there are various different biological and pathological aspects to their disease progression. Yet, it remains largely unclear which genetic factors underlie well-established sex differences in Alzheimer’s disease. This proposal will fill in this gap by using a series of state-of-the-art innovative approaches to discover sex-specific genetic risk variants for Alzheimer’s disease, including performing the largest sex-stratified genome-wide association study of Alzheimer’s disease to date, studying for the first time the role of X-chromosome and sex-specific rare variant effects on Alzheimer’s disease, and using rich proteomics data to discover new Alzheimer’s disease risk genes. Across these lines of research, we will also identify how measures of hormone exposure contribute to sex-specific genetic risk for Alzheimer’s disease. Findings from this work will help gain important insights into the pathophysiology of Alzheimer’s disease, identify novel sex-specific risk factors relevant to personalized genetic medicine, and uncover potential new Alzheimer’s disease drug targets that may more optimally benefit both sexes.
Developmental research project (2022) 3.2
Principal investigator: Igor Feinstein, PhD, Clinical Assistant Professor, Division of Adult Cardiothoracic Anesthesiology, Department of Anesthesiology, Perioperative and Pain Medicine
Title: Comprehensive Biomarker Analysis of Perioperative Neurocognitive Disorder and its Relationship to Latent Alzheimer’s Disease Pathology
Project description: Over 500,000 open heart procedures are performed in the United States annually. While these procedures have become progressively safer, it is notable that a large proportion of patients undergoing these major surgical procedures suffer from some degree of postoperative cognitive dysfunction, classified as a Perioperative Neurocognitive Disorder (PND). An increasing body of evidence suggests that PND shares a common biological basis with the pathology underlying Alzheimer’s disease (AD) and that major surgical stress may unmask latent neurodegenerative processes and lead to symptomatic deficits. This study aims to examine whether open heart surgery exacerbates AD-related processes by characterizing the effect of open heart surgery on levels of plasma p-tau181, an accessible and highly sensitive and specific biomarker predictive of early AD. Plasma p-tau181 levels will be measured at multiple perioperative time points before, during and after cardiac surgery together with biomarkers of neuronal injury (neurofilament light, NfL), comprehensive CSF molecular analyses and longitudinal cognitive testing. Key analyses will test whether preoperative p-tau181, NfL and CSF biomarker levels correlate with pre and postoperative cognitive function, whether surgery-induced increases in p-tau181, NfL, and CSF biomarker levels correlate with surgery-associated postoperative cognitive decline, and whether increases are different depending on APOE genotype. Expected findings of p-tau181 being correlated with postoperative cognitive deficits will establish this biomarker as having utility in reliably identifying patients predisposed to or at risk for postoperative cognitive decline and/or the development of AD after surgery. This will, in turn, allow for larger-scale studies that ultimately aim at individualizing clinical care pathways based on a patient’s vulnerability or resilience to surgery-induced cognitive decline and for studying modifiable risk factors and interventional approaches.
Developmental research project (2022) 3.3
Principal investigator: Caleb Lareau, PhD, Instructor, Department of Pathology
Title: Single synaptosome sequencing
Project description: Synapses are the fundamental structural and functional unit in the human brain that mediates neuronal communication and underlie key cognitive traits such as learning and memory. Impaired synaptic function has been linked to many neurodegenerative disorders, but the mechanisms underlying this dysfunction have not been fully characterized. Notably, synaptic communication is an energy-demanding largely driven by mitochondria, which are recruited to synapses, and previous studies have identified an increased burden of somatic mitochondrial DNA (mtDNA) mutations in the brain of individuals with neurodegenerative disorders.
Our project combines expertise of pioneering methods that isolate individual synapses (termed Synaptosomes) with genomics technology development. Thus, the goal of this project is to establish a new technology to identify somatic mitochondrial mutations in millions of single synaptosomes from frozen human brain tissue, including from patients with preclinical and clinical neurodegenerative. Our approach will enable a multi-omic readout that will further reveal the molecular phenotype of individual synaptosomes, linking somatic mutations to neuronal state, and revealing the impact of somatic variation in mtDNA on the pathogenesis of neurodegeneration.
Developmental research project (2021) 2.1
Principal investigator: Andrew Gentles, PhD, Assistant Professor, Depts of Medicine (Biomedical Informatics Research) and Biomedical Data Sciences
Title: Cell type specific transcriptional changes in neurodegenerative disease
Project description: Understanding changes in gene expression in specific cell types between normal and diseased brain is crucial for understanding disease mechanisms and identifying novel therapeutic targets. Recovering cell type specific gene expression from tissues is also a major first step towards reconstructing cell specific transcriptional networks, and inferring cross-talk between cell types in disease states. Single cell RNA-seq is widely used, but it is expensive and requires extensive sample processing, which can distort cellular content in tissues and perturb their functional states. Bulk RNA-seq can be applied cost-effectively to large cohorts of clinically annotated patient samples, including archival materials, but it conceals cell type specific changes in gene expression between normal and diseased brain tissue. Computational deconvolution methods applied to gene expression data from bulk tissues can estimate the proportion of different cell types in the mixture and recover cell type specific gene expression data. This approach opens the possibility of identifying cell type specific differences in gene expression between normal and disease tissues without dissociation and single cell processing. We propose to optimize such approaches for the cell types present in brain and validate them for human and mouse in silico. We will deconvolute bulk RNA-seq from human samples with known “ground truth” determined by CODEX (CODetection by indEXing) proteomic imaging. We will then apply this framework to large clinically-annotated data cohorts acquired from normal brain and neurodegenerative disease. We will focus on Alzheimer disease and vascular dementia to identify specific hypotheses that will be experimentally testable by collaborators at the Stanford ADRC.
Developmental research project (2021) 2.2
Principal investigator: Harini Iyer, PhD, Postdoctoral scholar, Developmental Biology
Title: Lysosomal signaling in microglia and Alzheimer’s disease
Project description: Genome-wide association studies of Alzheimer’s disease (AD) patient mutations implicate immune pathways in disease onset or progression. Microglia, the primary immune cells residing in the brain, ensure nervous system well-being and function by eliminating dying cells, pruning neural connections, and orchestrating appropriate immune responses. Two key microglial processes – lysosomal activity and inflammatory response – are aberrantly involved in neurodegenerative diseases, but it is not known how these microglial activities become dysfunctional in AD. My preliminary studies demonstrate the importance of two key lysosomal transcription factors, Tfeb and Tfe3 (Tfeb/3), in the function and maintenance of microglia in zebrafish. Although zebrafish cannot be directly used to study AD pathology, their advantages include amenability to live imaging, feasibility of large-scale mutagenesis screens, and optical transparency of embryos. Furthermore, culturing microglia in vitro results in rapid loss of microglial identity. Human TFEB/3 may regulate immune genes in macrophages (progenitors of microglia), and TFEB/3 may be dysregulated in AD. However, the extent to which disruption of TFEB/3 activity in microglia contributes to the pathology in AD is not known.
I have defined a lysosomal regulatory circuit acting upstream of Tfeb/3 in microglia, and in the next phase of my training, I will identify downstream targets of Tfeb/3 using RNAseq in loss and gain of function mutants. I will compare differentially expressed genes to publicly available AD databases. I will use CRISPR mutagenesis to show how Tfeb/3 activity is disrupted in AD to uncover the functions of Tfeb/3 targets. These experiments will advance my training in CRISPR/CRISPRa screens, analysis of AD patient databases, methods to identify and image microglia in vivo, and assays of microglial function (e.g., engulfment and elimination of neuronal debris). Disruption of microglia activity in AD is well appreciated, but a large-scale functional genomic screen of genes associated with AD mutations has not yet been performed.
As an independent researcher, I will capitalize on my training in microglial imaging and lysosomal biology to study genes associated with patient mutations in AD. I will identify zebrafish homologs of genes mutated in AD, prioritize them based on microglial expression or lysosomal function, and perform CRISPR knockout or CRISPRa gene activation, followed by characterization of microglial responses. My proposed research renders microglial biology accessible to live imaging and functional characterization in vivo, and it bridges the gap between genomic resources available for AD and the cellular and molecular mechanisms underlying the pathology of this devastating disease.
Developmental research project (2020) 1.1
Principal investigator: Monther Abu-Remaileh, PhD
Title: Molecular basis of lysosomal dysfunction in neurodegeneration
Project description: Lysosomes are small compartments within nerve cells where macromolecules and damaged organelles are degraded and cleared. Lysosomes serve as major regulators of cell signaling, metabolism and longevity; and lysosomal dysfunction is implicated in causing Alzheimer’s disease and Parkinson’s disease. There is an urgent need to understand the molecular and biochemical basis of lysosomal dysfunction in age-associated neurodegenerative diseases to determine its role in disease pathology. This is a challenging task, because there are few tools to probe the protein, small molecule, and RNA contents of lysosomes. To overcome this hurdle, we recently developed a method to immunopurify lysosomes from cells and tissues, a method we call LysoIP. Purified lysosomes are suitable for small molecule profiling using liquid chromatography and mass spectrometry. In this proposal, we hypothesize that lysosomal dysfunction drives age-associated neurodegeneration. By profiling lysosomes from cells derived from skin biopsies of patients with Alzheimer’s disease and Parkinson’s disease, we will determine the exact biochemical basis of lysosomal dysfunction in these two disorders. We have three aims:
Aim 1: Using our innovative technology, we will generate LysoTag fibroblasts obtained from Alzheimer’s disease and Parkinson’s disease patients enrolled in the Stanford Alzheimer's Disease Research Center.
Aim 2: We will profile the metabolome, lipidome and proteome of tagged lysosomes purified from fibroblasts of patients with Alzheimer’s disease and Parkinson’s disease, and we will determine the biochemical basis of lysosomal dysfunction in these disorders.
Aim 3: We will determine the consequences of the lysosomal changes we discover in order to understand the biochemical basis of neurotoxicity in Alzheimer’s disease and Parkinson’s disease. Using functional approaches, we will determine the role of altered lysosomal pathways in disease pathology.
Developmental research project (2020) 1.2
Principal investigator: Heather E. Moss, MD, PhD
Title: Retinal biomarkers of Alzheimer’s disease and related diseases
Project description: Development of effective therapies for Alzheimer’s disease and related diseases has been hampered by lack of biomarkers to facilitate early diagnosis of disease and measure early treatment response. The retina is a promising tissue in which to identify biomarkers of neurological diseases because the retina is comprised of neural tissue and can be imaged non-invasively in vivo with high resolution. Historical attempts to leverage in vivo imaging derived retinal measurements in patients with neurological diseases for clinical advantage has been stymied by lack of specificity, which we believe is due to low resolution of clinical retinal imaging modalities. Accordingly, this application seeks to apply state-of-the-art retinal imaging technology to discover features in the retinas of human subjects with mild cognitive impairment and Alzheimer’s disease that can be developed as biomarkers for early detection of Alzheimer’s disease and measurement of Alzheimer’s disease progression. We hypothesize that there are specific retinal changes associated with Alzheimer’s disease and that these can be detected using in-vivo ophthalmic imaging. Subjects with Alzheimer’s disease, mild cognitive impairment and healthy controls will undergo cellular-level retinal imaging with adaptive optics scanning laser ophthalmoscopy. Structural retinal features unique to Alzheimer’s disease and mild cognitive impairment subjects will be identified through comparison with control subjects. Categorical and continuous measures of retinal structural features will be correlated with baseline cognitive testing, neuroimaging and cerebrospinal fluid measures collected for Alzheimer’s disease and mild cognitive impairment subjects through the Alzheimer’s Disease Research Center as well as with changes in these measures during the year after retinal imaging. The immediate impact of this project will be to identify specific retinal features in living humans that are candidates for detection of neurodegeneration and progression of neurodegeneration in Alzheimer’s disease. The features will have direct translational potential as biomarkers that are relevant to human disease and practical for measurement in living humans. In the longer term these will serve as the foundation for new directions for Alzheimer’s disease research in humans, including developing interventions to prevent and treat Alzheimer’s disease.
REC fellowship project 4.1
Principal investigator: Mable Lam, PhD, Postdoctoral Fellow, Department of Neurosurgery
Title: Myelin modulation of neuronal activity in Alzheimer’s disease
Project description: Loss of white matter occurs during early stages of Alzheimer’s disease and correlates with cognitive decline. White matter largely consists of myelin, a fatty substance that propagates electrical signaling along nerve fibers. Myelin is important for numerous brain functions, including cognition and memory, but how myelin dysfunction arises in Alzheimer’s disease (AD) is unclear. I will generate myelin-forming cells and neurons that have the genetic background of individuals with and without AD to study how they differ in electrical activity on a multielectrode array. Developing this assay will allow us to determine cell-based markers of AD prognosis and screen for small molecules or biologics that rescue AD-related cellular dysfunction.
REC fellowship project 4.2
Principal investigator: April May, PhD, Postdoctoral Scholar, Palo Alto VA MIRECC and the Department of Psychiatry and Behavioral Sciences at Stanford University School of Medicine
Title: A comprehensive examination of the contribution of alcohol consumption to the progression from mild cognitive impairment to dementia
Project description: The global population is aging and older adults (OA) are consuming alcohol at greater rates than previous generations. As we age, numerous biological changes occur, including decline in cognition, alterations in brain structure, and a diminished ability to process and eliminate alcohol, resulting in higher concentrations for longer periods of time, putting OA at greater risk for impairment. Although alcohol use is believed to exacerbate these naturally occurring biological changes with age, this relationship is not well understood. Therefore, to expand our knowledge of this relationship, this project aims to execute a comprehensive examination of the contribution of alcohol consumption on the progression to Alzheimer’s disease and related dementias (ADRD) and the associated impact on cognitive performance and brain structure among OA with mild cognitive impairment (MCI). This examination will contribute to our understanding of ADRD and has clinical implications for our patients, as alcohol use is a modifiable behavior.
REC fellowship project 3.1
Principal Investigator: Alesha Heath, PhD, Postdoctoral Fellow, Department of Psychiatry and Behavioral Sciences
Title: Contribution of genetics to variable sleep disturbances in Alzheimer's disease
Project description: Those diagnosed with Alzheimer’s disease (AD) express a variable symptom base which may further contribute to cognitive decline or be protective against the neurodegeneration caused by this disorder. Sleep is one of these variables symptoms. As sleep is a critical regulator of both memory consolidation and the clearance of the toxic byproducts thought to be involved in AD pathology, disturbed sleep highly contributable to the progression of AD. Aspects of sleep architecture are known to be heritable and influenced by underlying genetics. Therefore, this project will expand on this past research, taking advantage of recently available large-scale whole genome sequencing and advances in tandem repeat genotyping to examine the association of multiple types of polymorphisms to sleep disturbances in a large AD database. By identifying genetic associations which could allow for early detection of sleep disturbances that accelerate the progression of this disorder, this will open up avenues to apply early interventions and monitor the progression of this symptom closely.
REC fellowship project 3.2
Principal investigator: Jeff Nirschl, M.D., Ph.D., Neuropathology Fellow and post-doctoral researcher, Department of Pathology
Title: Deep phenotyping neuropathologic changes and transcriptomics in Alzheimer's disease with and without comorbid Lewy body disease
Project description: Alzheimer’s disease (AD) and Lewy body disease (LBD) pathologies often coexist, but the common molecular pathways underlying neurodegeneration in these disorders remain unclear. Neuropathologic evaluation remains essential to characterize the diverse spectrum of neuropathologic change and co-pathologies. Despite advances in computer vision and whole-slide imaging (WSI), standardized neuropathology reporting relies on manual, semi-quantitative measurements that require expert review and are subject to inter-observer variability. Further, traditional metrics ignore the complex, hierarchical interaction among neurons, glia, and co-pathologies (tangles, plaques, Lewy bodies) within microscopic brain regions. This proposal will develop novel deep learning algorithms to quantify detailed neuropathologic features from WSI and will also leverage spatial transcriptomics to characterize the unique and shared transcriptomic signatures in AD and AD+ LBD. This work will improve our understanding of the continuum of pathology in AD and LBD as well as reveal shared molecular pathways that underly neuron loss and degeneration in these devastating diseases.
REC fellowship project 2.1
Principal investigator: Ramy Hussein, PhD, Postdoctoral Fellow, Department of Radiology
Title: Multimodal Deep Learning for Medical Imaging and Clinical Data Fusion: Paving the Way for Better Prediction and Prognosis of Alzheimer’s Disease
Project description: Dementia is the loss of cognitive functioning (thinking, remembering, and reasoning) and behavioral abilities to such an extent that it interferes with a person’s daily life and activities. Worldwide, around 50 million people have dementia, and there are nearly 10 million new cases every year. Alzheimer’s disease is the most common cause of dementia among older adults. Mild cognitive impairment (MCI) is the intermediary stage condition between the expected cognitive decline of normal aging and the more serious decline of Alzheimer’s disease and other dementias. Around one third of MCI individuals progress to dementia within 3 years following the initial diagnosis. Identifying the MCI individuals at high risk of developing Alzheimer’s disease is crucial for fighting against this disease. Thus, we are developing a variety of multimodal Artificial Intelligence algorithms that can effectively integrate heterogeneous sources of medical data to achieve more reliable and accurate predictions of Alzheimer’s disease, and also increase our understanding of which source(s) of medical data have the greatest impact on the prediction performance. This will help achieve better prognosis of Alzheimer’s disease and also reduce burdens on data collection and patient burnout in clinical practice.
REC fellowship project 2.2
Principal investigator: Joe Winer, PhD, Postdoctoral fellow, Department of Neurology & Neurological Sciences
Title: Characterizing relationships between sleep-wake rhythms, neuroinflammation, and cognition in neurodegenerative disease"
Project description: Sleep and daytime activity patterns are known to change across the lifespan, and both are affected in neurodegenerative disease. New research suggests that these changes are not only symptoms of disease, but may affect cognition and disease progression. Actigraphy watches, which use technology similar to the accelerometers in our phones, can be used to collect sleep-wake activity data outside the laboratory. This project will collect actigraphy data from healthy older adults, patients with Alzheimer's disease, and patients with Lewy body disease enrolled at the Stanford ADRC in order to characterize patterns of sleep-wake activity across disease severity. These data will be combined with cognitive assessments and disease biomarkers in order to investigate the contribution of sleep-wake dysfunction to cognitive decline and inflammatory dysregulation in the progression of both Alzheimer's and Lewy body disease.
REC fellowship project 1.1
Principal investigator: Ehsan Adeli, PhD, Clinical Assistant Professor, Department of Psychiatry and Behavioral Sciences
Title: Data-driven stratification of neurodegenerative disorders using video-MRI analysis
Project description: Video recordings of patient movements are commonly used to assess the physical impact of disease as patient are assessed with the Movement Disorders Society-Unified Parkinson's Disease Rating Scale or as the Short Physical Performance Battery. Traditionally, videos are then reviewed by medical experts, who categorize the movements in a relatively coarse, imprecise manner. In this project, we propose to quantify movements automatically from video recordings and extract video-based digital biomarkers of neurodegenerative diseases. These digital biomarkers will then be related to neural systems obtained from MRI images of the brain. This procedure can automatically relate movement patterns to brain circuitry underlying these movements.
REC fellowship project 1.2
Principal investigator: Tammy Tran, PhD, Postdoctoral fellow, Department of Psychology
Title: Molecular and imaging biomarkers underlying neurodegeneration in aging
Project description: Neuropathological changes emerge decades prior to clinical manifestation in Alzheimer’s disease. Early cognitive decline may be predicted by several pathophysiological abnormalities, detectable by in vivo biomarkers early in the disease trajectory. These include the presence of molecular and imaging biomarkers for tau and amyloid. Cognitive decline may also be predicted by cortical thinning across medial temporal lobe regions, particularly in entorhinal cortex and CA1-SRLM, a sublayer that serves as an interface between entorhinal cortex and other hippocampal subfields. Using high-precision metrics (high resolution 3T and ultra-high resolution 7T MRI), I will examine neurodegeneration (including subregion-specific cortical thickness and hippocampal volume) in relation to examine imaging biomarkers (Tau PET(F-PI2620)) and molecular biomarkers (e.g., Ab42/Ab40 ratio, pTau181, t-tau) and investigate how these promising biomarkers correspond to cognitive function in healthy older adults.
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Kim J, Schweizer TA, Fischer CE, Munoz DG. The role of cerebrovascular disease on cognitive and functional status and psychosis in severe Alzheimer’s disease. Journal of Alzheimer & ApoE disease. 2017;55(1):381-389. PMID: 27662301; PMCID: PMC5115606.
Lange C, Suppa P, Mäurer A, Ritter K, Pietrzyk U, Steinhagen-Thiessen E, Fiebach JB, Spies L, Buchert R. Mental speed is associated with the shape irregularity of white matter MRI hyperintensity load. Brain Imaging and Behavior. 2017;11(6):1720-1730. PMID: 27796731; PMCID: PMC5843991.
Latimer CS, Keene CD, Flanagan ME, Hemmy LS, Lim KO, White LR, Montine KS, Montine TJ. Resistance to Alzheimer disease neuropathologic changes and apparent cognitive resilience in the nun and Honolulu-Asia aging studies. Journal of Neuropathology and Experimental Neurology. 2017;76(6):458-466. PMID: 28499012.
Lim YY, Mormino EC; Alzheimer's Disease Neuroimaging Initiative. ApoE genotype and early β-amyloid accumulation in older adults without dementia. Neurology. 2017;89(10):1028-1034. PMID: 28794245; PMCID: PMC5589795.
Mathur V, Burai R, Vest RT, Bonanno LN, Lehallier B, Zardeneta ME, Mistry KN, Do D, Marsh SE, Abud EM, Blurton-Jones M, Li L, Lashuel HA, Wyss-Coray T. Activation of the STING-dependent Type I interferon response reduces microglial reactivity and neuroinflammation. Neuron. 2017;96(6):1290-1302.e6. PMID: 29268096; PMCID: PMC5806703.
Moga DC, Taipale H, Tolppanen AM, Tanskanen A, Tiihonen J, Hartikainen S, Wu Q, Jicha GA, Gnjidic D. A comparison of sex differences in psychotropic medication use in older people with Alzheimer’s disease in the US and Finland. Drugs & Aging. 2017;34(1):55-65. PMID: 27896799; PMCID: PMC5253689.
Moga DC, Abner EL, Wu Q, Jicha GA. Bladder antimuscarinics and cognitive decline in elderly patients. Alzheimer’s & Dementia. 2017;3(1):139-148. PMID: 28462390; PMCID: PMC5408467.
Moheb N, Mendez MF, Kremen SA, Teng E. Executive dysfunction and behavioral symptoms are associated with deficits in instrumental activities of daily living in frontotemporal dementia. Dementia and Geriatric Cognitive Disorders. 2017;43(1-2):89-99. PMID: 28103593; PMCID: PMC5300022.
Montgomery V, Harris K, Stabler A, Lu LH. Effects of delay duration on the WMS logical memory performance of older adults with probable Alzheimer’s disease, probable vascular dementia, and normal cognition. Archives of Clinical Neuropsychology. 2017;32(3):375-380. PMID: 28431036; PMCID: PMC5400025.
Neu SC, Pa J, Kukull W, Beekly D, Kuzma A, Gangadharan P, Wang LS, Romero K, Arneric SP, Redolfi A, Orlandi D, Frisoni GB, Au R, Devine S, Auerbach S, Espinosa A, Boada M, Ruiz A, Johnson SC, Koscik R, Wang JJ, Hsu WC, Chen YL, Toga AW. Apolipoprotein E genotype and sex risk factors for Alzheimer disease: a meta-analysis. JAMA Neurology. 2017;74(10):1178-1189. PMID: 28846757; PMCID: PMC5759346.
Ng B, Varoquaux G, Poline JB, Thirion B, Greicius MD, Poston KL. Distinct alterations in Parkinson’s medication-state and disease-state connectivity. NeuroImage. Clinical. 2017;16:575-585. PMID: 28971008; PMCID: PMC5608603.
Pandya SY, Lacritz LH, Weiner MF, Deschner M, Woon FL. Predictors of reversion from mild cognitive impairment to normal cognition. Dementia and Geriatric Cognitive Disorders. 2017;43(3-4):204-214. PMID: 28301848; PMCID: PMC5495561.
Postupna N, Latimer CS, Larson EB, Sherfield E, Paladin J, Shively CA, Jorgensen MJ, Andrews RN, Kaplan JR, Crane PK, Montine KS, Craft S, Keene CD, Montine TJ. Human striatal dopaminergic and regional serotonergic synaptic degeneration with Lewy Body Disease and inheritance of APOE ε4. American Journal of Pathology. 2017;187(4): 884-895. PMID: 28212814; PMCID: PMC5397713.
Ramsey CM, Gnjidic D, Agogo GO, Allore H, Moga D. Longitudinal patterns of potentially inappropriate medication use following incident dementia diagnosis. Alzheimer’s & Dementia. 2017;4:1-10. PMID: 29296658; PMCID: PMC5738721.
Ritter AR, Leger GC, Miller JB, Banks SJ. Neuropsychological testing in pathologically verified Alzheimer disease and frontotemporal dementia: How well do the Uniform Data Set measures differentiate between diseases? Alzheimer Disease and Associated Disorders. 2017;31(3):187-191. PMID: 28005562; PMCID: PMC5479762.
Sano M, Zhu CW, Grossman H, Schimming C. Longitudinal cognitive profiles in diabetes: results from the National Alzheimer's Coordinating Center's Uniform Data. Journal of the American Geriatrics Society. 2017;65(10):2198-2204. PMID: 28771679; PMCID: PMC5641239.
Schmidt SA, Ording AG, Horváth-Puhó E, Sørensen HT, Henderson VW. Non- melanoma skin cancer and risk of Alzheimer’s disease and all-cause dementia. PloS ONE. 2017;12(2): e0171527. PMID: 28225789; PMCID: PMC5321271.
Sennik S, Schweizer TA, Fischer CE, Munoz DG. Risk factors and pathological substrates associated with agitation/aggression in Alzheimer’s disease: A preliminary study using NACC data. Journal of Alzheimer’s Disease. 2017;55(4):1519-1528. PMID: 27911311; PMCID: PMC5607738.
Tchakoute CT, Sainani KL, Henderson VW. Semantic memory in the clinical progression of Alzheimer disease. Cognitive and Behavioral Neurology. 2017;30(3):81-89. PMID: 28926415; PMCID: PMC5617354.
Tripodis Y, Alosco ML, Zirogiannis N, Gavett BE, Chaisson C, Martin B, McClean MD, Mez J, Kowall N, Stern RA. The effect of traumatic brain injury history with loss of consciousness on rate of cognitive decline among older adults with normal cognition and Alzheimer’s disease dementia. Journal of Alzheimer's Disease. 2017;59(1):251-263. PMID: 28655133; PMCID: PMC5614490.
Qian J, Hyman BT, Betensky RA. Neurofibrillary tangle stage and the rate of progression of Alzheimer symptoms: modeling using an autopsy cohort and application to clinical trial design. JAMA Neurology. 2017;74(5):540-548. PMID: 28288263; PMCID: PMC5547572.
Andreasson KI, Bachstetter AD, Colonna M, Ginhoux F, Holmes C, Lamb B, Landreth G, Lee DC, Low D, Lynch MA, Monsonego A, O’Banion MK, Pekny M, Puschmann T, Russek-Blum N, Sandusky LA, Selenica ML, Takata K, Teeling J, Town T, Van Eldik LJ. Targeting innate immunity for neurodegenerative disorders of the nervous system. Journal of Neurochemistry. 2016; 138(5):653-93. PMID: 27248001; PMCID: PMC5433264.
Bonham LW, Geier EG, Fan CC, Leong JK, Besser L, Kukull WA, Kornak J, Andreassen OA, Schellenberg GD, Rosen HJ, Dillon WP, Hess CP, Miller BL, Dale AM, Desikan RS, Yokoyama JS. Age-dependent effects of APOE ε4 in preclinical Alzheimer’s disease. Annals of Clinical and Translational Neurology. 2016;3(9):668-77. PMID: 27648456; PMCID: PMC5018579.
Burke SL, Maramaldi P, Cadet T, Kukull W. Neuropsychiatric symptoms and Apolipoprotein E: associations with eventual Alzheimer’s disease development. Archives of Gerontology and Geriatrics. 2016;65:231-8. PMID: 27111252; PMCID: PMC5029123.
Day GS, Musiek ES, Roe CM, Norton J, Goate AM, Cruchaga C, Cairns NJ, Morris JC. Phenotypic similarities between late-onset autosomal dominant and sporadic Alzheimer disease: a single-family case-control study. JAMA Neurology. 2016;73(9):1125-32. PMID: 27454811; PMCID: PMC5025942.
Henderson VW, St John JA, Hodis HN, McCleary CA, Stanczyk FZ, Shoupe D, Kono N, Dustin L, Allayee H, Mack WJ. Cognitive effects of estradiol after menopause: a randomized trial of the timing hypothesis. Neurology. 2016;87(7):699-708. PMID: 27421538; PMCID: PMC4999165.
Jaeger PA, Lucin KM, Britschgi M, Vardarajan B, Huang RP, Kirby ED, Abbey R, Boeve BF, Boxer AL, Farrer LA, Finch N, Graff-Radford NR, Head E, Hoffree M, Huang R, Johns H, Karydas A, Knopman DS, Loboda A, Masliah E, Narasimhan R, Petersen RC, Podtelezhnikov A, Pradhan S, Rademakers R, Sun CH, Younkin SG, Miller BL, Ideker T, Wyss-Coray T. Network-driven plasma proteomics expose molecular changes in the Alzheimer’s brain. Molecular Neurodegeneration. 2016;11:31. PMID: 27112350; PMCID: PMC4845325.
Karim R, Dang H, Henderson VW, Hodis HN, St John J, Brinton RD, Mack WJ. Effect of reproductive history and exogenous hormone use on cognitive function in mid- and late life. Journal of the American Geriatrics Society. 2016;64(12):2448- 2456. PMID: 27996108; PMCID: PMC5180359.
Middeldorp J, Lehallier B, Villeda SA, Miedema SS, Evans E, Czirr E, Zhang H, Luo J, Stan T, Mosher KI, Masliah E, Wyss-Coray T. Preclinical assessment of young blood plasma for Alzheimer disease. JAMA Neurology. 2016;73(11):1325-1333. PMID: 27598869; PMCID: PMC5172595.
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Rettberg JR, Dang H, Hodis HN, Henderson VW, St John JA, Mack WJ, Brinton RD. Identifying postmenopausal women at risk for cognitive decline within a healthy cohort using a panel of clinical metabolic indicators: potential for detecting an at-Alzheimer’s risk metabolic phenotype. Neurobiology of Aging. 2016;40:155-63. PMID: 26973115; PMCID: PMC4921204.
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Developmental project applications
Application Deadline April 10, 2023
Request for Developmental Project applications that address scientific issues on inequities and ethno-racial differences in risks, manifestations, and outcomes for Alzheimer’s disease and related disorders
Iqbal Farrukh and Asad Jamal Stanford Alzheimer’s Disease Research Center (ADRC)
Developmental Projects on Alzheimer’s disease and Alzheimer’s disease related disorders (AD/ADRD)
$150,000 (anticipated project period: 6/1/23-3/31/25)
Deadline extended: April 10, 2023 11:00pm
This RFP is also available on this webpage:
Amount of funding and budget information:
Applicants may request up to $150,000 in direct costs for over one and a half years (expires 3/31/25) under this program. The Stanford ADRC plans to fund up to two developmental projects this year, based on the number and scientific quality of applications. The budget period is anticipated to begin 06/01/2023-3/31/2025, pending NIA approval.
All Stanford faculty (UTL, UML, NTL-Research, CE), Instructors, and post-doctoral fellows.
This funding mechanism is intended to allow an investigator the opportunity to develop robust preliminary data sufficient to provide the basis for an application for independent research support from the NIH or other agency. Developmental project grants are designed for 1) for junior faculty investigators, as are postdoctoral fellows or instructors transitioning to an academic position (or the equivalent) at Stanford (this grant is non-transferable). and 2) for more senior investigators who have experience in areas other than Alzheimer’s disease or Lewy body research, and who want to work in the Alzheimer research field broadly defined or want to try a new hypothesis, method, or approach that is not an extension of ongoing Alzheimer or Lewy body research.
Individuals from racial, ethnic, or other groups that are underrepresented in biomedical research, as well as individuals with disabilities, are encouraged to apply. The expectation is that proposed research will allow the investigator to develop preliminary data sufficient for the basis of an application for independent support. You do not have to submit your application through your RPM.
An investigator is eligible only once for development project support.
Senior ADRC faculty are not eligible to submit applications but may be included as unfunded collaborators.
Note: a PI waiver will be required for non-faculty successful applicants. PI waivers would need to be approved by the appropriate schools or Dean of Research. For School of Medicine PIs, requests must be made to the Research Management Group (RMG). For PIs outside of the school of Medicine, the individual must work with their school dean’s office. Postdoctoral fellows in senior, academic trajectory can apply as PI if Co-PI is faculty advisor/mentor who is UTL, UML, NTL-Research, CE who will in turn be responsible for all oversight, budget and reporting requirements of the project.
The Stanford ADRC focuses on Alzheimer’s disease (AD), mild cognitive impairment, Parkinson’s disease, Lewy body disease, and healthy aging. We seek proposals addressing issues related to inequities and ethno-racial differences in AD risk, manifestations, and outcomes, including but not limited to innovative research (basic, clinical, behavioral, translational, epidemiologic, caregiving, or educational) likely to advance our understanding of the impacts of health disparities in Alzheimer’s and related dementias and aid in prevention or treatment; or enhance caregiving, community outreach and education.
Example areas can include health disparities in stress processes and exposure to adversity, cost and/or access to care, education and geographic disparities, structural racism, diagnosis and assessment procedures, disparities in caregiving and dementia care, biology of AD, analyses of pathways that create and sustain AD disparities and others. Those investigating novel methods of recruitment and engagement of minoritized populations, as well as advancement of methods to capture the complex interplay of social determinants of health and their impact on health outcomes are also welcome. For more details on the National Institute of Aging emphasis on health disparities, please see here. (https://www.nia.nih.gov/research/dbsr/ad-adrd/disparities).
Preference is given to proposals that use data and resources from the Stanford ADRC, including clinical data, biological specimens (e.g., blood, DNA, CSF, stool microbiome, skin fibroblasts, autopsy tissues), imaging data (including structural MR and amyloid-PET), and biostatistical resources; or that use data and resources of the National Alzheimer Coordinating Center (https://www.alz.washington.edu/), National Centralized Repository for AD (NCRAD) (https://ncrad.iu.edu/), and the National Institute on Aging Genetics of AD Data Storage (NIAGADS), (https://www.niagads.org/). Please be sure to address type of ADRC resources and how such resources will be used in your proposal. Note that direct access to Stanford ADRC participants is limited, and you will need to obtain approval from Center PI.
Programmatic questions should be directed to Dr. Katrin Andreasson, chair of the Developmental Project Review Committee (email@example.com), administrative questions to Nusha Askari (firstname.lastname@example.org), Senior Administrator of the ADRC.
If selected and funded:
Funding is contingent upon receipt of all required documents and protocols and approval by the NIA, and verification of approved protocols, (eg., IRB, if needed), should be submitted to Nusha Askari at the ADRC. An annual report and final progress report in NIH format will also be due to Nusha Askari. A presentation to the ADRC team and presentation of progress is required, usually at the time of the annual site visit of the ADRC External Advisory Board.
To submit an application:
By April 10, 2023, 11pm (deadline extended from 3/31/23 on 3/17/23), please submit one PDF file containing the following in the order listed below via email to: Nusha Askari, Stanford ARDC, email@example.com.
1) Title page
Stanford Alzheimer's Disease Research Center JEDI Developmental Projects 2023 (Year 4-5)
Project Leader Name, Title, department, address, phone number, email
Co-Investigator(s), if any: Name, Title, department, address, phone number, email
2) Project summary or abstract
Include project title (up to 30 lines)
3) Research proposal
Specific Aims and Research Strategy (consisting of Significance, Innovation, and Approach), together limited to 3 pages, including any tables and figures. Bibliography/References does not count against the 3-page limit. Use standard NIH page formatting. See above regarding citing how and what ADRC resources will be used.
4) Detailed budget
Up to $150,000 direct costs
Budget period: 06/01/23 to 03/31/25 (or other budget period, as appropriate).
Please note: You do not have to have your RPM prepare your budget now, but if approved we will need to submit an official budget to the NIH in January 2023 (the ADRC will do that).
5) Budget justification (1 page, NIH format)
6) NIH-format biosketch for the project leader and any co-investigators
For a template and sample biosketch see this NIH webpage: (effective January 2022) https://grants.nih.gov/grants/forms/biosketch.html https://grants.nih.gov/grants/guide/notice-files/NOT-OD-21-073.html
7) Other support (NIH format) for project leader and co-investigators Please include both active and pending support – follow new NIH guidelines: https://grants.nih.gov/grants/forms/othersupport.html
***When you email your application to Nusha Askari (firstname.lastname@example.org), please send via secure email. We welcome all eligible investigators, per above guidelines.
We would appreciate if you would add in the body of your email your self-identified sex/gender and race and ethnicity, if applicable. This is voluntary information requested by the NIA for our reporting purposes in our annual report – they would like to know the representation of all of our applicants, where possible. We appreciate your understanding and will try to limit access to this information via summaries etc. where possible.
The ADRC Developmental Project Review Committee will review and recommend action on all
Developmental Project applications. You will receive a notification of selection by May 2023.
The goal is to bring in junior faculty and senior faculty not currently working in AD/ADRD research, with a focus on health disparities, and our review process prioritizes these groups. We will consider other applicants as well, depending on the number of quality applications we receive.
Note: the release of funds after selection is contingent upon formal approval of the National Institute on Aging and verification by ADRC of the recipient's human subject, SCRO, and animal subject approvals and compliance with other administrative issues.
For any non-faculty awardees, before funding can be released, as per Stanford policy, we will require a letter of support from the faculty mentor or department chair who will have oversight of expenditures via Stanford's system.
Research Education Component (REC) fellowship applications
Application Deadline March 10, 2023
The Stanford Alzheimer’s Disease Research Center (ADRC) at Stanford University School of Medicine is now accepting applications for a one to two-year Research Fellowship. The Stanford ADRC is part of a nationwide network of Alzheimer’s Disease Centers supported by the National Institutes of Health. The centers work together to translate research advances into improved diagnosis and care for people with Alzheimer’s disease and Alzheimer’s disease related dementias (AD/ADRD). The clinical and research focus of the Stanford ADRC includes both Alzheimer’s disease and Lewy body diseases (dementia with Lewy bodies and Parkinson’s disease). Our center has particular strength in neuroimmunity, synapse biology, brain imaging, clinical assessment and clinical research, biostatistics and bioinformatics, epidemiology, and caregiver outreach. As such, the Stanford ADRC Research Fellowship provides specialized training in AD/ADRD.
The mission of the Stanford ADRC Research Fellowship Program is to prepare the next generation of researchers for careers in brain aging and AD/ADRD though participation in integrated clinical and basic science training opportunities and mentored research experiences. In collaboration with their mentors, Scholars accepted into the Stanford ADRC Research Fellowship Program will develop and implement a research project, present and publish findings, participate in grant writing, and learn to use the latest technologies for educational activities and clinical service delivery. Our Scholars receive mentorship in AD and ADRD from internationally renowned clinical and basic science researchers. Please see Appendix A for a listing of Faculty Mentors.
Stanford ADRC Research Fellowship Faculty Interests (for complete list see: https://med.stanford.edu/adrc/people.html
His research focuses on brain–behavior relations, on risk factors for cognitive aging and dementia, and on interventions to help prevent and treat these disorders. Within the population health sciences, his research agenda encompasses cognitive change that occurs as a usual concomitant of normal aging and more debilitating impairment that accompanies Alzheimer’s disease, dementia with Lewy bodies, and other forms of dementia.
The Wyss-Coray research team studies brain aging and neurodegeneration with a focus on age-related cognitive decline and Alzheimer’s disease. The lab is following up on earlier discoveries which showed circulatory blood factors can modulate brain structure and function and factors from young organisms can rejuvenate old brains. Current studies focus on the molecular basis of this systemic communication with the brain by employing a combination of genetic, cell biology, and proteomics approaches in model organisms and humans.
His interests include translational research in neurodegenerative disease therapeutics. His research team is developing new drugs that are focused on the modulation of fundamental cell signaling pathways that are involved in neurodegeneration.
Dr. Yesavage directs several programs designed to examine changes in mental function across the lifespan. In particular we are concerned with Alzheimer's Disease (senile dementia), Age-Associated Cognitive Decline (normal changes in cognitive function seen in older adults) and cognitive training to reduce the loss, depression in aging, sleep disorders in aging and lifespan changes in complex tasks such as aircraft pilot performance.
We are investigating the role that innate immune responses play in the initiation and progression of neurological diseases. Through a systems biology approach, we are identifying novel immune pathways that may play critical roles in maladaptive brain inflammation, and we are working to understand how these responses cause neurodegeneration and circuit disruption.
Her research program combines her background in diagnostic neuropathology, knowledge of developmental neuroscience, and state-of-the-art cellular and molecular technologies to advance the understanding of Alzheimer’s disease and related dementias. She is currently applying single-cell methods to human brain to dissect the contributions of distinct cell types to Alzheimer’s disease pathogenesis and investigate the mechanisms of tau-mediated neurodegeneration in human brain.
The focus of the Montine Laboratory is on the structural and molecular bases of cognitive impairment with the goal of defining key pathogenic steps and thereby new therapeutic targets.
His research interests include (1) Survival Analysis and Semiparametric Modeling, (2) Resampling Methods, (3) Meta Analysis, (4) High Dimensional Data Analysis, and (5) Precision Medicine for Disease Diagnosis, Prognosis and Treatment.
His research is concentrated in the area of statistical genetics and integrative analysis of omics data, with the aim of developing novel statistical and computational methodologies for the identification and interpretation of complex biological pathways involved in human diseases, particularly neurological disorders. His methodology interest includes high-dimensional data analysis, correlated (longitudinal, familial) data analysis and machine learning algorithms.
Her research focus is on developing artificial intelligence and machine learning algorithms to enable new capabilities in biomedicine and healthcare. She has extensive expertise in deep learning and computer vision, and has developed computer vision algorithms for analyzing diverse types of visual data ranging from video capture of human behavior, to medical images and cell microscopy images.
Dr. Greicius' research focuses on elucidating the neurobiologic underpinnings of AD. His lab combines cutting edge brain imaging, "deep" phenotyping, and whole-genome sequencing of human subjects to identify novel pathways involved in AD pathogenesis.
We are interested in multimodal approaches to understand aging and neurodegenerative disease in humans. Our research aims to measure the earliest brain changes that occur before clinical symptoms are present, with the overall goal of leveraging this data to understand cognitive aging, contribute to early detection, and improve the ability to predict the onset of future clinical impairment.
A nationally recognized leader in geriatrics and palliative care, Periyakoil founded and directs Stanford Aging, Geriatrics and Ethnogeriatrics transdisciplinary collaborative center (SAGE Center), the Ethno-geriatrics & the Successful Aging Project, and the Palliative Care portal and the Letter Project.
The Wellness in Aging lab seeks to reduce the negative effect of late life cognitive impairment through the development and evaluation of nonpharmacological, activity-based interventions for at-risk groups.
The Poston Lab seeks to understand the underlying brain circuitry associated with movement disorders, such as Parkinson’s disease, and in particular the changes in this circuitry that lead to specific symptoms, including both motor symptoms and cognitive/behavioral symptoms.
Dr. Sha’s is Associate Vice Chair of Clinical Research and Director of the Behavioral Neurology Fellowship. Her clinical time is devoted to caring for patients with Alzheimer’s disease and other neurodegenerative disorders and her research is devoted to finding treatments for these cognitive disorders. She runs the Clinical Trials Program for the Division of Behavioral Neurology.
Funding and Eligibility
The Stanford ADRC Research Fellowship is funded by the NIA and the Stanford ADRC. The current annual stipend at the Stanford ADRC is up to $30,000 annually. Funds can be used for a variety of purposes including, but not limited to, salary/benefits, funds for coursework or travel to ADRC meetings, and funds for research project-related expenses, if applicable and as the budget permits. Budgeted items must be scientifically justified as essential for a successful fellowship.
Applications will be accepted from two categories: (1) Junior Faculty: defined as an instructor or assistant professor, who have completed an MD and/or PhD with clinical residency/fellowship and/or post-doctoral training, (2) Trainees: clinical fellows (behavioral neurology, movement disorders, psychiatry, neuropsychology, geriatrics, palliative care) post-doctoral research fellows, residents (neurology, psychiatry, geriatrics), graduate students and medical students.
The Stanford ADRC strongly believes in the value of diversity in our training program and we are focused on recruiting and supporting individuals from all backgrounds. We encourage applications from candidates that are underrepresented in medicine, economically disadvantaged, and whose backgrounds or experiences would diversify our clinical field.
Research Fellowship Structure
This fellowship consists of one to two calendar years of training; Scholars start on or around March 1 each year. The length of the proposed training (1 or 2 years) must be scientifically justified as essential for a successful fellowship. At the beginning of the training year, the Scholar will work with the Research Mentor and REC Leadership to develop an individualized training plan that balances taking advantage of the rich training and professional development opportunities with conducting clinical and basic science research in AD and ADRD. An example Training Plan can be found in Appendix B.
Research Opportunities and Expectations
Each Scholar is expected to actively participate in research during their training tenure with the Fellowship. Scholars work collaboratively with their Research mentor to: a) identify or develop meaningful clinical research projects that address key areas within AD and ADRD research b) identify roles on ongoing clinical research projects (including the numerous ongoing projects available at the Stanford ADRC) that may foster the advanced development of both clinical and research skills; and c) participate in the development and submission of empirical manuscripts, grants and other scholarly projects focused on the AD and ADRD.
Applicants are strongly encouraged to consider the use of existing data and biospecimen resources within the Stanford ADRC as well as data of the National Alzheimer’s Coordinating Center when designing their clinical research projects. Scholars are expected to complete a meaningful research project during their Fellowship, and to consistently show clear markers of their research productivity. Key markers of productivity may include a) the development of a grant proposal; b) generating scientific manuscript and submitting it for publication; and c) presentation of this project at a professional meeting, or some other marker of productivity.
Stanford ADRC Research Scholars have the opportunity to participate in many didactics throughout the training year. There are several Core and Optional year-long didactics Scholars will participate in as part of the ADRC (see Table 1), as well as training in Responsible Conduct of Research (if not already completed as part of other training). There are additional didactics Scholars can choose to include in their training plan, including courses in statistics, epidemiology, laboratory methods, image processing, or other topics relevant to their projects and training goals.
TABLE 1. Didactics / Coursework and Clinical Research Training*
ADRC Consensus meeting
Small Group Discussion
1.5 hours, bi-monthly
ADRC Clinical Core
Behavioral Neurology Case Review Conference
Small Group Discussion
1 hour, Weekly
ADRC Clinical Core and the Memory Disorders Center
ADRC/Udall Distinguished Speaker Series
1 hour, monthly
ADRC Admin Core
BIO 98 — Understanding Alzheimer’s Disease and Dementia
ADRC Clinical Core Faculty
ADRC Clinical Pathological Conference
Lecture, Small Group Discussion
2 hours, quarterly
ADRC Neuropathology Core
MED 255/225C: Responsible Conduct of Research
Lecture, Small Group Discussion
Stanford Center for Biomedical Ethics
The REC Scholar will meet with a member of the REC Leadership team monthly to review the Scholar’s progress towards meeting the goals set for in the Scholar’s Training Plan. This meeting will serve as an opportunity for the Scholar and REC leaders to identify any potential areas for adjustment in the Training Plan, to ensure that the full breadth of experience leading to independence in all competency areas will be obtained by the end of the training period. The training plan will be formally assessed and revised annually.
Application and Selection Process
Selection of REC Scholars is done by the REC Selection Committee using the following criteria:
- Breadth and quality of previous general training experience
- Breadth, depth, and quality of training experience areas relevant to the Stanford ADRC mission
- Quality and scope of scholarship, as indicated partially by research, convention papers, and publications
- Relationship between clinical and research interests/experience of the applicant
- Evidence of personal maturity and accomplishments
- Thoughtfulness of answers to the application questions
- Goodness of fit between the applicant’s stated objectives and the training program and medical center’s resources
- Use of ADRC resources
- Strength of letters of recommendation from professionals who know the applicant well
The Fellowship program follows a policy of selecting the most qualified candidates and is an Equal Opportunity Employer. Our commitment to diversity includes attempting to ensure an appropriate representation of individuals along many dimensions, including (but not limited to) gender, sexual orientation, age, ethnic/racial minorities, and persons with disabilities.
To apply to be a Stanford ADRC Research Scholar, you must submit the required application elements listed below. Incomplete applications will not be read by the REC Selection Committee.
Application Requirements List:
1. A signed letter of interest (up to 3 pages) that strictly follows the instructions. Please review the Stanford ADRC website so that you are familiar with the faculty and research interests. In your letter please describe
- Your previous educational, clinical and research experiences
- Your areas of clinical and research interest and its alignment with the Stanford ADRC research area(s) and mission
- Specific clinical and research goals and objectives for your Fellowship Year
- Your career “next steps”
2. NIH Biosketch
3. Research Proposal (up to 3 pages, not including references)
- Project Title
- Purpose: state the goal and specific objectives of the proposed research; clearly describe the question to be addressed. Also indicate the length of fellowship proposed (1 or 2 years) with brief justification.
- Background: Explain scientific rationale for project; describe innovative features of your project; describe how research will advance knowledge in AD and ADRD field.
- Methods and Research Plan: Outline proposed study design methods.
- Key Personnel: Identify Research Mentor and other potential collaborators. ADRC Faculty are not required to be the primary research mentor, but are encouraged to be collaborator or part of the mentorship team.
- Resources Needed with Associated Costs: Proposed use of funds (up to $30,000) and scientific justification for the proposed project.
4. Two letters of recommendation from faculty members or clinical supervisors who know your research work well. We encourage letter writers to send documents as Microsoft Word or Adobe Acrobat files.
Informational Webinar available [recorded and available on the ADRC website: http://med.stanford.edu/adrc/research/fellowship.html]
January 2022: Applications open
March 10, 2023: 5:00 PM PST: Application Deadline, Apply:
March 20 2023: Review of Applications and Notification of Funding Decisions
April 1, 2023: Fellowships begin
January 2024: ADRC External Advisory Council Meeting
March 31, 2024: End of First Training Year, Annual Reports due
Informational Webinar for ADRC REC Fellowship
ADRC research projects, 2015-2019
Large research project 1
Principal investigator: Thomas C. Südhof, MD
Title: Synaptic function of gamma-secretase and AD: role of neurexins and neuroligins
Large research project 2
Principal investigator: Kathleen L. Poston, MD, MS
Title: Working memory in Parkinson disease: a cognitive and systems neuroscience approach
Pilot research project (2019) 5.1
Principal investigators: Marion Buckwalter, MD, PhD
Title: StrokeCog-LP: adaptive immune responses in vascular dementia and Alzheimer's disease
Pilot research project (2019) 5.2
Principal investigators: Vinod Menon, PhD
Title: Leveraging big data and using deep learning neural networks to classify subtypes of cognitive deficits in Parkinson's disease and Alzheimer's disease
Pilot research project (2019) 5.3
Principal investigator: Marius Wernig, MD, PhD
Title: Role of microglia during brain aging
Pilot research project (2018) 4.1
Principal investigators: Ami S. Bhatt, MD, PhD
Title: Dissecting the role of intestinal microbes in neurodegeneration
Pilot research project (2018) 4.2
Principal investigators: Philippe Mourrain, PhD
Title: Sleep management for improved synaptic and behavioral functions in Alzheimer's disease
Pilot research project (2018) 4.3
Principal investigators: Gregory Zaharchuk, MD, PhD and Elizabeth Mormino, PhD
Title: Extreme radiation dose reduction for PET imaging of Alzheimer's disease using deep learning
Pilot research project (2017) 3.1
Principal investigator: Edward D. Plowey, MD, PhD
Title: Role of brainstem taupathy in early Alzheimer's disease
Pilot research project (2017) 3.2
Principal investigator: Emmanuel Mignot, MD, PhD
Title: Genome-wide association study to map CSF protein expression quantitative trait loci(eQTL) in Alzheimer's disease
Pilot research project (2016) 2.1
Principal investigators: Anne Brunet, PhD and Daniel F. Jarosz, PhD
Title: Developing the African killifish as a new system to model the age-dependency, genetics, and spread of Alzheimer’s disease
Pilot research project (2015) 1.1
Principal investigators: Michael Bassik, PhD and Aaron D. Gitler, PhD
Title: Identification of regulators of α-synuclein toxicity using high complexity shRNA and CRISPR/sgRNA screens
Pilot research project (2015) 1.2
Principal investigator: Michael Zeineh, MD, PhD
Title: In Vivo MR microscopic imaging of Alzheimer's disease at 7T