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.
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 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.
Arendt JFH, Horváth-Puhó E, Sørensen HT, Nexø E, Pedersen L, Ording AG, Henderson VW. Plasma vitamin B12 levels, high-dose vitamin B12 treatment, and risk of dementia. Journal of Alzheimer’s disease. 2021; 79(4):1601-1612. PubMed PMID: 33459639; PubMed Central PMCID: PMC7990402.
Asprec L, Blinderman CD, Berlin A, Callahan ME, Widera E, Periyakoil VS, Smith AK, Nakagawa S. Virtual interinstitutional palliative care consultation during the COVID-19 pandemic in New York City. Journal of Palliative Medicine. 2021. 24(9):1387-1390; PubMed PMID: 34191591; PubMed Central PMCID: PMC8590147 (available on 2022-09-01).
Belloy ME, Eger SJ, Le Guen Y, Napolioni V, Deters KD, Yang HS, Scelsi MA, Porter T, James SN, Wong A, Schott JM, Sperling RA, Laws SM, Mormino EC, He Z, Han SS, Altmann A, Greicius MD; A4 Study Team; Insight 46 Study Team; Australian Imaging Biomarkers and Lifestyle (AIBL) Study; Alzheimer's Disease Neuroimaging Initiative. KL*VS heterozygosity reduces brain amyloid in asymptomatic at-risk APOE*4 carriers. Neurobiology of Aging. 2021; 101:123-129. PubMed PMID: 33610961; PubMed Cental PMCID: PMC8122023 (available on 2022-05-01).
Cano MT, Pennington DL, Reyes R, Pineda BS, Llamas JA, Periyakoil VS, Muñoz RF. Factors associated with smoking in low-income persons with and without chronic illness. Tobacco Induced Disorders, 2021: 19-59. PubMed PMID 34305505; PubMed Central PMCID: PMC8280622.
Carlson ML, Toueg TN, Khalighi MM, Castillo J, Shen B, Azevedo EC, DiGiacomo P, Mouchawar N, Chau G, Zaharchuk G, James ML, Mormino EC, Zeineh MM. Hippocampal subfield imaging and fractional anisotropy show parallel changes in Alzheimer's disease tau progression using simultaneous tau-PET/MRI at 3T. Alzheimer’s Dementia (Amst). 2021;13(1):e12218. PubMed PMID: 34337132; PubMed Central PMCID: PMC8319659.
Chavda R, Cao JS, Benge JF. Neuropsychological impact of white matter hyperintensities in older adults without dementia. Applied Neuropsychology: Adult. 2021; 28(3):354-362. PubMed PMID: 31287337; PubMed Central PMCID: PMC6949427.
Chittoor-Vinod VG, Nichols RJ, Schüle B. Genetic and environmental factors influence the pleomorphy of LRRK2 Parkinsonism. International Journal of Molecular Science. 2021; 22(3):1045. PubMed PMID:33494262; PubMed Central PMCID: PMC7864502.
Cholerton BA, Poston KL, Yang L, Rosenthal LS, Dawson TM, Pantelyat A, Edwards KL, Tian L, Quinn JF, Chung KA, Hiller AL, Hu SC, Montine TJ, Zabetian CP. Semantic fluency and processing speed are reduced in non-cognitively impaired participants with Parkinson's disease. Journal of Clinical Experimental Neuropsychology. 2021;43(5):469-480. PubMed PMID: 34355669; PubMed Central PMCID: PMC8376799.
deRochemonteix M, Napolioni V, Sanyal N, Belloy M, Caporaso NE, Landi MT, Greicius M, Chatterjee N, Han SS. A likelihood ratio test for gene environment interaction based on the trend effect of genotype under an additive risk model using the gene0environment independence assumption. American Journal of Epidemiology. 2021;190(1):129-141. PubMed PMID:32870973; PubMed Central (in process).
Deters KD, Napolioni V, Sperling RA, Greicius MD, Mayeux R, Hohman T, Mormino EC. Amyloid PET imaging in self-identified non-Hispanic Black participants of the anti-amyloid in asymptomatic Alzheimer’s disease (A4) study. Neurology. 2021; 96(11):e1491-e1500. PubMed PMID: 33568538; PubMed Central PMCID: PMC8032379.
Feinstein I, Wilson EN, Swarovski MS, Andreasson KI, Angst MS, Greicius MD. Plasma Biomarkers of Tau and Neurodegeneration During Major Cardiac and Non-cardiac Surgery. JAMA Neurology. 2021 Nov 1;78(11):1407-1409. PubMed PMID: 34542578; PubMed Central PMCID: PMC8453356.
Gajera CR, Fernandez R, Montine KS, Fox EJ, Mrdjen D, Postupna NO, Keene CD, Bendall SC, Montine TJ. Mass-tag barcoding for multiplexed analysis of human synaptosomes and other anuclear events. Cytometry Annals. 2021;99(9):939-945. Pub Med PMID: 33818911; PubMed Central PMCID: PMC8590852 (available on 2022-09-01).
He Z, Le Guen Y, Liu L, Lee J, Ma S, Yang AC, Liu X, Rutledge J, Losada PM, Song B, Belloy ME, Butler RR 3rd, Longo FM, Tang H, Mormino EC, Wyss-Coray T, Greicius MD, Ionita-Laza I. Genome-wide analysis of common and rare variants via multiple knockoffs at biobank scale, with an application to Alzheimer disease genetics. American Journal of Human Genetics. 2021; 108(12):2336-2353. PubMed PMID: 34767756; PubMed Central PMCID: PMC8715147.
He Z, Liu L, Wang C, Le Guen Y, Lee J, Gogarten S, Lu F, Montgomery S, Tang H, Silverman EK, Cho MH, Greicius M, Ionita-Laza I. Identification of putative causal loci in whole-genome sequencing data via knockoff statistics. Nat Commun. 2021 May 25;12(1):3152. PubMed PMID: 34035245; PubMed Central PMCID: PMC8149672.
Johnson AL, Nystrom NC, Piper ME, Cook J, Norton DL, Zuelsdorff M, Wyman MF, Flowers Benton S, Lambrou NH, O'Hara J, Chin NA, Asthana S, Carlsson C, Gleason CE. Cigarette smoking status, cigarette exposure, and duration of abstinence predicting incident dementia and death: a multi-state model approach. Journal of Alzheimer’s Disease. 2021; 80(3):1013-1023. PubMed PMID: 33646160; PubMed Central PMCID: PMC8044009.
Kiselica AM, Benge JF. Quantitative and qualitative executive dysfunction in frontotemporal and Alzheimer’s dementia. Applied Neuropsychology: Adult. 2021; 28(4):449-463. PubMed PMID: 31424275; PubMed Central PMCID: PMC7028481.
Kunkle BW, Schmidt M, Klein HU, Naj AC, Hamilton-Nelson KL, Larson EB, Evans DA, De Jager PL, Crane PK, Buxbaum JD, Ertekin-Taner N, Barnes LL, Fallin MD, Manly JJ, Go RCP, Obisesan TO, Kamboh MI, Bennett DA, Hall KS, Goate AM, Foroud TM, Martin ER, Wang LS, Byrd GS, Farrer LA, Haines JL, Schellenberg GD, Mayeux R, Pericak-Vance MA, Reitz C, Graff-Radford NR, Martinez I, Ayodele T, Logue MW, Cantwell LB, Jean-Francois M, Kuzma AB, Adams LD, Vance JM, Cuccaro ML, Chung J, Mez J, Lunetta KL, Jun GR, Lopez OL, Hendrie HC, Reiman EM, Kowall NW, Leverenz JB, Small SA, Levey AI, Golde TE, Saykin AJ, Starks TD, Albert MS, Hyman BT, Petersen RC, Sano M, Wisniewski T, Vassar R, Kaye JA, Henderson VW, DeCarli C, LaFerla FM, Brewer JB, Miller BL, Swerdlow RH, Van Eldik LJ, Paulson HL, Trojanowski JQ, Chui HC, Rosenberg RN, Craft S, Grabowski TJ, Asthana S, Morris JC, Strittmatter SM, Kukull WA. Novel Alzheimer disease risk loci and pathways in African-American individuals using the African genome resources panel: a meta-analysis. JAMA Neurology. 2021; 78(1):102-113. PubMed PMID: 33074286; PubMed Central PMCID: PMC7573798.
Lee S, Hussein R, Ward R, Jane Wang Z, McKeown MJ. A convolutional-recurrent neural network approach to resting-state EEG classification in Parkinson’s disease. Neuroscience Methods. 2021; 361:109282. PubMed PMID: 34237382; PubMed Central PMCID: PMC8528094.
Le Guen Y, Belloy ME, Napolioni V, Eger SJ, Kennedy G, Tao R, He Z, Greicius MD; Alzheimer’s Disease Neuroimaging Initiative. A novel age-informed approach for genetic association analysis in Alzheimer’s disease. Alzheimer’s Research & Therapy. 2021; 13(1):72. PubMed PMID: 33794991; PubMed Central PMCID: PMC8017764.
Le Guen Y, Napolioni V, Belloy ME, Yu E, Krohn L, Ruskey JA, Gan-Or Z, Kennedy G, Eger SJ, Greicius MD. Common x-chromosome variants are associated with Parkinson disease risk. Annals of Neurology.2021l;90(1):22-34. PubMed PMID: 33583074; PubMed Central PMCID: PMC8601399.
Lu M, Zhao Q, Poston KL, Sullivan EV, Pfefferbaum A, Shahid M, Katz M, Kouhsari LM, Schulman K, Milstein A, Niebles JC, Henderson VW, Fei-Fei L, Pohl KM, Adeli E. Quantifying Parkinson’s disease motor severity under uncertainty using MDS-UPDRS videos. Medical Image Analysis. 2021; 73:102179. PubMed PMID: 34340101; PMCID: PMC8453121 (available on 2022-10-01).
Minhas PS, Latif-Hernandez A, McReynolds MR, Durairaj AS, Wang Q, Rubin A, Joshi AU, He JQ, Gauba E, Liu L, Wang C, Linde M, Sugiura Y, Moon PK, Majeti R, Suematsu M, Mochly-Rosen D, Weissman IL, Longo FM, Rabinowitz JD, Andreasson KI. Restoring metabolism of myeloid cells reverses cognitive decline in ageing. Nature. 2021;590(7844): 122-128. PubMed PMID: 33473210; PubMed Central PMCID: PMC8274816.
Mormino EC, Toueg TN, Azevedo C, Castillo JB, Guo W, Nadiadwala A, Corso NK, Hall JN, Fan A, Trelle AN, Harrison MB, Hunt MP, Sha SJ, Deutsch G, James M, Fredericks CA, Koran ME, Zeineh M, Poston K, Greicius MD, Khalighi M, Davidzon GA, Shen B, Zaharchuk G, Wagner AD, Chin FT. Tau PET imaging with (18)F-PI-2620 in aging and neurodegenerative diseases. European Journal of Nuclear Molecular Imaging. 2021;48:2233-2244.PubMed PMID: 7755737; PubMed Central PMCID:PMV7755737.
Morrison LJ, Periyakoil VS, Arnold RM, Tucker R, Chittenden E, Sanchez-Reilly S, Carey EC. Launching the next steps to improve hospice and palliative medicine fellow performance assessment: a look back to the initial toolkit of assessment methods. Journal of Pain Symptom Management. 2021; 61(3):613-627. PubMed PMID: 33091584; PubMed Central PMCID: PMC7569474.
Napolioni V, Scelsi MA, Khan RR, Altmann A, Greicius MD. Recent consanguinity and outbred autozygosity are associated with increased risk of late-onset Alzheimer’s disease. Frontiers in Genetics. 2021; 11:629373. PubMed PMID: 33584820; PubMed Central PMCID: PMC7879576.
Nørgaard M, Horváth-Puhó E, Corraini P, Sørensen HT, Henderson VW. Sleep disruption and Alzheimer’s disease risk: Inferences from men with benign prostatic hyperplasia. EClinical Medicine. 2021; 32:100740. PubMed PMID: 33681742; PubMed Central PMCID: PMC7910709.
Oh H, Leventhal O, Channappa D, Henderson VW, Wyss-Coray T, Lehallier B, Gate D. Methods to investigate intrathecal adaptive immunity in neurodegeneration. Molecular Degeneration. 2021;16(1):3. PubMed PMID: 33482851; PubMed Central PMCID: PMC7824942.
Park VT, Kim A, Cho IH, Nam B, Nguyen K, Vuong Q, Periyakoil VS, Hong YW. Motivation to participate in precision health research and acceptability of texting as a recruitment and intervention strategy among Vietnamese Americans: Qualitative study. JMIR Mhealth UHealth, 2021; 9(3):e230508. PubMed PMID:33704080; PubMed Central PMCID: PMC7995081.
Pershing S, Goldstein MK, Henderson VW, Bundorf MK, Lu Y, Rahman M, Stein JD. Receipt of eye care services among Medicare beneficiaries with and without dementia. Opthalmology. 2020; 127(8): 1000- 1011. PubMed PMID:32317179; PubMed Central PMCID: PMC7384939.
Phongpreecha T, Gajera CR, Liu CC, Vijayaragavan K, Chang AL, Becker M, Fallahzadeh R, Fernandez R, Postupna N, Sherfield E, Tebaykin D, Latimer C, Shively CA, Register TC, Craft S, Montine KS, Fox EJ, Poston KL, Keene CD, Angelo M, Bendall SC, Aghaeepour N, Montine TJ. Single-synapse analyses of Alzheimer's disease implicate pathologic tau, DJ1, CD47, and ApoE. Scientific Advances. 2021;7(51):eabk0473. PubMed PMID: 34910503; PubMed Central PMCID: PMC8673771.
Reith FH, Mormino EC, Zaharchuk G. Predicting future amyloid biomarkers in dementia patients with machine learning to improve clinical trial patient selection. Alzheimer’s Dementia (NY). 2021;7(1):e12212. PubMed PMID: 34692985; PubMed Central PMCID: PMC8515556.
Ryman SG, Yutsis M, Tian L, Henderson VW, Montine TJ, Salmon DP, Galasko D, Poston KL. Cognition at each stage of Lewy Body Disease with co-occurring Alzheimer’s disease pathology. Journal of Alzheimer’s Disease. 2021;80(3):1243-1256. PubMed PMID: 33646154; PubMed Central PMCID: PMC8150665.
Sanyal N, Napolioni V, de Rochemonteix M, Belloy ME, Caporaso NE, Landi MT, Greicius MD, Chatterjee N, Han SS. A robust test for additive gene-environment interaction under the trend effect of genotype using an empirical Bayes-type shrinkage estimator. American Journal of Epidemiology. 2021 Sep 1;190(9):1948-1960. PubMed PMID: 33942053; PubMed Central PMCID: PMC8579053.
Sayed N, Huang Y, Nguyen K, Krejciova-Rajaniemi Z, Grawe AP, Gao T, Tibshirani R, Hastie T, Alpert A, Cui L, Kuznetsova T, Rosenberg-Hasson Y, Ostan R, Monti D, Lehallier B, Shen-Orr SS, Maecker HT, Dekker CL, Wyss-Coray T, Franceschi C, Jojic V, Haddad F, Montoya JG, Wu JC, Davis MM, Furman D. An inflammatory aging clock (iAge) based on deep learning tracks multimorbidity, immunosenescence, frailty and cardiovascular aging. Nature Aging. 2021;1:598-615. PubMed PMID: 34888528; PubMed Central PMCID: PMC8654267.
Scelsi MA, Napolioni V, Greicius MD, Altmann A; Alzheimer’s Disease Neuroimaging Initiative (ADNI) and the Alzheimer’s Disease Sequencing Project (ADSP). Network propagation of rare variants in Alzheimer’s disease reveals tissue-specific hub genes and communities. PLoS Computational Biology. 2021; 17(1): e1008517. PubMed PMID: 33411734; Pub Med Central PMCID: PMC7817020.
Tran EM, Stefanick ML, Henderson VW, Rapp SR, Chen JC, Armstrong NM, Espeland MA, Gower EW, Shadyab AH, Li W, Stone KL, Pershing S. Association of visual impairment with risk of incident dementia in a women’s health initiative population. JAMA Opthalmology. 2020; 138(6):624-633. PubMed PMID:32297918; PubMed Central PMCID: PMC7163778.
Trelle AN, Carr VA, Wilson EN, Swarovski MS, Hunt MP, Toueg TN, Tran TT, Channappa D, Corso NK, Thieu MK, Jayakumar M, Nadiadwala A, Guo W, Tanner NJ, Bernstein JD, Litovsky CP, Guerin SA, Khazenzon AM, Harrison MB, Rutt BK, Deutsch GK, Chin FT, Davidzon GA, Hall JN, Sha SJ, Fredericks CA, Andreasson KI, Kerchner GA, Wagner AD, Mormino EC. Association of CSF biomarkers with hippocampal- dependent memory in preclinical Alzheimer disease. Neurology. 2021; 96(10):e1470-1481. PubMed PMID: 33408146; PubMed Central PMCID: PMC8055319 (available on 2022-03-09).
Wilson EN, Andreasson KI. TAM-ping down amyloid in Alzheimer disease. Nature Immunology. 2021;22(5):543-544. PubMed PMID:33859407; PubMed Central PMCID: PMC8549633.
Wilson EN, Swarovski MS, Linortner P, Shahid M, Zuckerman AJ, Wang Q, Channappa D, Minhas PS, Mhatre SD, Plowey ED, Quinn JF, Zabetian CP, Tian L, Longo FM, Cholerton B, Montine TJ, Poston KL, Andreasson KI. Soluble TREM2 is elevated in Parkinson's disease subgroups with increased CSF tau. Brain: a journal of neurology. 2020;143(3):932-943. PubMed PMID: 32065223; PubMed Central PMCID: PMC7089668.
Winer JR, Deters KD, Kennedy G, Jin M, Goldstein-Piekarski A, Poston KL, Mormino EC. Association of short and long sleep duration with amyloid-β burden and cognition in aging. JAMA Neurology. 2021: 78(10):1187-1196. PubMed PMID: 34459862; PubMed Central PMCID: PMC8406215 (available on 2022-08- 30).
Xiong C, Luo J, Coble D, Agboola F, Kukull W, Morris JC. Complex interactions underlie racial disparity in the risk of developing Alzheimer's disease dementia. Alzheimer’s Dementia. 2020 Apr;16(4):589-597. PubMed PMID: 32067357; PubMed Central PMCID: PMC7259475.
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Developmental project applications
Application Deadline November 15, 2021
Asad Jamal and Iqbal Farrukh Stanford Alzheimer’s Disease Research Center (ADRC)
Developmental Projects for Alzheimer’s disease and Alzheimer’s disease related disorders (AD/ADRD) ($250,000)
The Alzheimer’s Disease Research Centers are a nationwide network of congressionally mandated Centers of Excellence supported by the National Institutes of Health
Deadline: November 15, 2021
This RFP is also available on this webpage: https://seedfunding.stanford.edu/apply/F7A2
Amount of funding and budget information:
Applicants may request up to $250K in direct costs for two years (range, one-to-three years) under this program. The Stanford ADRC plans to fund two developmental projects this year. The budget period is anticipated to begin 04/01/2022 (however may be later, pending NIA approval).
All Stanford faculty (UTL, UML, NTL-Research, CE). Awards are intended primarily for junior faculty investigators, but senior faculty investigators whose research is primarily in areas other than AD/ADRD are eligible, as are senior postdoctoral fellows or instructors transitioning to an academic position (or the equivalent). The expectation is that proposed research will allow the investigator to develop preliminary data sufficient for the basis of an application for independent support. An investigator is eligible only once for development project support. You do not have to submit your applications through your RPM.
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, mild cognitive impairment, Parkinson’s disease, Lewy body disease, and healthy aging. Proposals should describe innovative basic, clinical, behavioral, translational, epidemiologic, caregiving, or educational research likely to advance the understanding of the basic and clinical underpinnings of Alzheimer’s disease and related cognitive disorders (including Lewy body neurocognitive disorders); aid in prevention or treatment; or enhance caregiving, community outreach and education. 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.
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) junior faculty level investigators 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.
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 verification of approved protocols 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 November 15, 2021, 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
Alzheimer's Disease Research Center Developmental Projects 2022 (Year 3)
Project Leader Name, Title, department, address, phone number, email
Co-Investigator(s): 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 $250,000 direct costs (usually split evenly across the years; pending satisfactory progress in year 1)
Budget period: 04/01/22 to 03/31/24 (or other one to three-year 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 2022 (the ADRC will do that).
5) Budget justification (1 page, NIH format)
6) NIH-format biosketch for the project leader and co-investigators
For a template and sample biosketch see this NIH webpage: (see new changes in effect for January 2022)
7) Other support (NIH format) for project leader and co-investigators
Please include both active and pending support – follow new NIH guidelines:
The ADRC Developmental Project Review Committee will review and recommend action on all Developmental Project applications. You will receive a notification of selection by early January 2022.
The goal is to bring in junior faculty and senior faculty not currently working in AD/ADRD research, 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 February 14, 2022
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.
December 2021: Applications open
February 14 2022: 5:00 PM PST: Application Deadline
February 2022: Review of Applications and Notification of Funding Decisions
March 1, 2022: Fellowships begin
January 2023: ADRC External Advisory Council Meeting
February 28, 2023: End of First Training Year, Reports due
Please join the Informational Webinar on January 11th for more information and a chance to ask any questions regarding this Fellowship. Further information can also be obtained by contacting the Stanford ADRC Research Education Component Team, including our Coordinator Kristen Wheeler by email at firstname.lastname@example.org, or REC Lead Dr. Kathleen Poston by email at email@example.com or REC Co-Lead Dr. Kaci Fairchild by email at firstname.lastname@example.org.
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
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