Home town: Omaha, Nebraska

Boards, Advisory Committees, Professional Organizations

  • Secretary, Stanford University Postdoctoral Association (2014 - Present)

Professional Education

  • Bachelor of Science, Doane College (2006)
  • Doctor of Philosophy, University of Nebraska Medical Center (2012)

Stanford Advisors

Research & Scholarship

Current Research and Scholarly Interests

I study both immunology and neuroscience. I am interested in the interplay of the immune system and the CNS during disease. In particular, alterations in the immune system during neurodegenerative diseases, how these changes may reflect etiology and progression of disease and how they can be used as bio-markers or targets of therapy are of keen interest.

Lab Affiliations


Graduate and Fellowship Programs

  • Immunology/Rheumatology (Fellowship Program)


Journal Articles

  • Neuromagnetic Evidence of Abnormal Movement-Related Beta Desynchronization in Parkinson's Disease. Cerebral cortex (New York, N.Y. : 1991) Heinrichs-Graham, E., Wilson, T. W., Santamaria, P. M., Heithoff, S. K., Torres-Russotto, D., Hutter-Saunders, J. A., Estes, K. A., Meza, J. L., Mosley, R. L., Gendelman, H. E. 2013


    Parkinson's disease (PD) is a neurodegenerative disorder associated with debilitating motor, posture, and gait abnormalities. Human studies recording local field potentials within the subthalamic nucleus and scalp-based electroencephalography have shown pathological beta synchronization throughout the cortical-basal ganglia motor network in PD. Suppression of such pathological beta synchronization has been associated with improved motor function, which may explain the effectiveness of deep-brain stimulation. We used magnetoencephalography (MEG) to investigate neural population-level beta responses, and other oscillatory activity, during a motor task in unmedicated patients with PD and a matched group of healthy adults. MEG is a noninvasive neurophysiological technique that permits the recording of oscillatory activity during movement planning, execution, and termination phases. Each of these phases was independently examined using beamforming to distinguish the brain areas and movement phases, where pathological oscillations exist during motor control. Patients with PD exhibited significantly diminished beta desynchronization compared with controls prior to and during movement, which paralleled reduced alpha desynchronization. This study is the first to systematically investigate neural oscillatory responses in PD during distinct stages of motor control (e.g. planning, execution, and termination) and indicates that these patients have significant difficulty suppressing cortical beta synchronization during movement planning, which may contribute to their diminished movement capacities.

    View details for DOI 10.1093/cercor/bht121

    View details for PubMedID 23645717

  • CD4+Regulatory and Effector/Memory T Cell Subsets Profile Motor Dysfunction in Parkinson's Disease JOURNAL OF NEUROIMMUNE PHARMACOLOGY Saunders, J. A., Estes, K. A., Kosloski, L. M., Allen, H. E., Dempsey, K. M., Torres-Russotto, D. R., Meza, J. L., Santamaria, P. M., Bertoni, J. M., Murman, D. L., Ali, H. H., Standaert, D. G., Mosley, R. L., Gendelman, H. E. 2012; 7 (4): 927-938


    Animal models and clinical studies have linked the innate and adaptive immune system to the pathology of Parkinson's disease (PD). Despite such progress, the specific immune responses that influence disease progression have eluded investigators. Herein, we assessed relationships between T cell phenotype and function with PD progression. Peripheral blood lymphocytes from two separate cohorts, a discovery cohort and a validation cohort, totaling 113 PD patients and 96 age- and environment-matched caregivers were examined by flow cytometric analysis and T cell proliferation assays. Increased effector/memory T cells (Tem), defined as CD45RO+ and FAS+ CD4+ T cells and decreased CD31+ and α4β7+ CD4+ T cells were associated with progressive Unified Parkinson's Disease Rating Scale III scores. However, no associations were seen between immune biomarkers and increased age or disease duration. Impaired abilities of regulatory T cells (Treg) from PD patients to suppress effector T cell function was observed. These data support the concept that chronic immune stimulation, notably Tem activation and Treg dysfunction is linked to PD pathobiology and disease severity, but not disease duration. The association of T cell phenotypes with motor symptoms provides fresh avenues for novel biomarkers and therapeutic designs.

    View details for DOI 10.1007/s11481-012-9402-z

    View details for Web of Science ID 000312363500022

    View details for PubMedID 23054369

  • Murine Motor and Behavior Functional Evaluations for Acute 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine(MPTP) Intoxication JOURNAL OF NEUROIMMUNE PHARMACOLOGY Hutter-Saunders, J. A., Gendelman, H. E., Mosley, R. L. 2012; 7 (1): 279-288


    Acute intoxication with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induces nigrostriatal neurodegeneration that reflects Parkinson's disease (PD) pathobiology. The model is commonly used for rodent studies of PD pathogenesis and diagnostics and for developmental therapeutics. However, tests of motor function in MPTP-intoxicated mice have yielded mixed results. This unmet need reflects, in part, lesion severity, animal variability, and the overall test sensitivity and specificity. In attempts to standardize rodent motor function and behavioral tests, mice were trained on the rotarod or habituated in an open field test chamber, and baseline performance measurements were collected prior to MPTP intoxication. One week following MPTP intoxication, motor function and behavior were assessed and baseline measurements applied to post-MPTP measurements with normalization to PBS controls. Rotarod and open field tests assessed in this manner demonstrated significant differences between MPTP- and saline-treated mice, while tests of neuromuscular strength and endurance did not. We conclude that the rotarod and open field tests provide reliable measures of motor function for MPTP-intoxicated mice.

    View details for DOI 10.1007/s11481-011-9269-4

    View details for Web of Science ID 000304164000022

    View details for PubMedID 21431472

  • Inflammation and Adaptive Immunity in Parkinson's Disease COLD SPRING HARBOR PERSPECTIVES IN MEDICINE Mosley, R. L., Hutter-Saunders, J. A., Stone, D. K., Gendelman, H. E. 2012; 2 (1)


    The immune system is designed to protect the host from infection and injury. However, when an adaptive immune response continues unchecked in the brain, the proinflammatory innate microglial response leads to the accumulation of neurotoxins and eventual neurodegeneration. What drives such responses are misfolded and nitrated proteins. Indeed, the antigen in Parkinson's disease (PD) is an aberrant self-protein, although the adaptive immune responses are remarkably similar in a range of diseases. Ingress of lymphocytes and chronic activation of glial cells directly affect neurodegeneration. With this understanding, new therapies aimed at modulating the immune system's response during PD could lead to decreased neuronal loss and improved clinical outcomes for disease.

    View details for DOI 10.1101/cshperspect.a009381

    View details for Web of Science ID 000314239200004

    View details for PubMedID 22315722

  • Pathways towards an effective immunotherapy for Parkinson's disease EXPERT REVIEW OF NEUROTHERAPEUTICS Hutter-Saunders, J. A., Mosley, R. L., Gendelman, H. E. 2011; 11 (12): 1703-1715


    Immunizations that target specific types of immune responses are used commonly to prevent microbial infections. However, a range of immune responses may prove necessary to combat the ravages of neurodegenerative diseases. The goal is to eliminate the 'root' cause of neurodegenerative disorders, misfolded aggregated proteins, while harnessing adaptive immune responses to promote neural repair. However, immunization strategies used to elicit humoral immune responses against aberrant brain proteins have yielded mixed success. While specific proteins can be cleared, the failures in halting disease progression revolve, in measure, around adaptive immune responses that promote autoreactive T cells and, as such, induce a meningoencephalitis, accelerating neurodegeneration. Thus, alternative approaches for protein clearance and neural repair are desired. To this end, our laboratories have sought to transform autoreactive adaptive immune responses into regulatory neuroprotective cells in Parkinson's disease. In this context, induction of immune responses against modified brain proteins serves to break immunological tolerance, while eliciting adaptive immunity to facilitate neuronal repair. How to harness the immune response in the setting of Parkinson's disease requires a thorough understanding of the role of immunity in human disease and the ways to modify such immune responses to elicit therapeutic gain. These are discussed in this review.

    View details for DOI 10.1586/ERN.11.163

    View details for Web of Science ID 000298851800012

    View details for PubMedID 22091596

  • BL-1023 IMPROVES BEHAVIOR AND NEURONAL SURVIVAL IN 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE-INTOXICATED MICE NEUROSCIENCE Hutter-Saunders, J. A., Kosloski, L. M., McMillan, J. M., Yotam, N., Rinat, T., Mosley, R. L., Gendelman, H. E. 2011; 180: 293-304


    The therapeutic potential of BL-1023, a chemical combination of L-3,4-dihydroxyphenylalanine (L-DOPA) and gamma-aminobutyric acid (GABA), was investigated in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intoxicated mice. Such animals exhibit nigrostriatal degeneration, characteristic of human Parkinson's disease. Drug was administered during and after the development of MPTP-induced nigrostriatal lesions followed by measures of motor function and behavior, surviving nigrostriatal dopaminergic neurons and termini, and striatal dopamine levels. When administered after lesion development, BL-1023 improved motor function of MPTP-mice as measured by rotarod, total floor and vertical plane movements, and stereotypic movements in open field activity tests compared to MPTP-mice without treatment. This also paralleled modest nigral dopaminergic neuronal protection. Such significant improvements in motor function, behaviors, and dopaminergic neuronal numbers were not seen when BL-1023 was administered during MPTP-induced lesion development. The data demonstrate select abilities of BL-1023 to increase dopaminergic neuronal survival and improve motor function in MPTP-mice.

    View details for DOI 10.1016/j.neuroscience.2011.02.015

    View details for Web of Science ID 000289395600030

    View details for PubMedID 21320578

  • Regulatory T Cells Attenuate Th17 Cell-Mediated Nigrostriatal Dopaminergic Neurodegeneration in a Model of Parkinson's Disease JOURNAL OF IMMUNOLOGY Reynolds, A. D., Stone, D. K., Hutter, J. A., Benner, E. J., Mosley, R. L., Gendelman, H. E. 2010; 184 (5): 2261-2271


    Nitrated alpha-synuclein (N-alpha-syn) immunization elicits adaptive immune responses to novel antigenic epitopes that exacerbate neuroinflammation and nigrostriatal degeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease. We show that such neuroimmune degenerative activities, in significant measure, are Th17 cell-mediated, with CD4(+)CD25(+) regulatory T cell (Treg) dysfunction seen among populations of N-alpha-syn-induced T cells. In contrast, purified vasoactive intestinal peptide induced and natural Tregs reversed N-alpha-syn T cell nigrostriatal degeneration. Combinations of adoptively transferred N-alpha-syn and vasoactive intestinal peptide immunocytes or natural Tregs administered to MPTP mice attenuated microglial inflammatory responses and led to robust nigrostriatal protection. Taken together, these results demonstrate Treg control of N-alpha-syn-induced neurodestructive immunity and, as such, provide a sound rationale for future Parkinson's disease immunization strategies.

    View details for DOI 10.4049/jimmunol.0901852

    View details for Web of Science ID 000274768900007

    View details for PubMedID 20118279

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