Bio

Professional Education


  • Master of Public Health, Univ Texas Health Science Ctr-Houston (2012)
  • B of Medicine and B of Surgery, Maharashtra University of Health Sciences (2006)

Stanford Advisors


Patents


  • Ahmad Salehi, Devsmita Das, Van Dang, Martha Millan Sanchez, Brian Medina. "United StatesMethod of improving cognitive function and increasing dendritic complexity in humans with Down syndrome", Leland Stanford Junior University, Jan 29, 2013

Research & Scholarship

Current Research and Scholarly Interests


My research interest is understanding the mechanisms behind cognitive dysfunction in neurological diseases and finding innovative treatment strategies for it. My current focus is on studying the neurobiology of cognitive dysfunction in Down Syndrome and developing a therapeutic strategy for the same.

Publications

Journal Articles


  • Formoterol, a Long-Acting β2 Adrenergic Agonist, Improves Cognitive Function and Promotes Dendritic Complexity in a Mouse Model of Down Syndrome Biological Psychiatry Dang, V., Medina, B., Das, D., Moghadam, S., Ashford, W., Salehi, A., et al 2013
  • Ascending monoaminergic systems alterations in Alzheimer's disease. Translating basic science into clinical care Neuroscience and Biobehavioral Reviews Trillo, L., Das, D., Hsieh, W., Ashford, W., Salehi, A., et al 2013; 37 (8): 1363-1379
  • Neurobiological Elements of Cognitive Dysfunction in Down Syndrome: Exploring the Role of APP BIOLOGICAL PSYCHIATRY Sanchez, M. M., Heyn, S. N., Das, D., Moghadam, S., Martin, K. J., Salehi, A. 2012; 71 (5): 403-409

    Abstract

    Down syndrome (DS) is the most common cause of cognitive dysfunction in children. Additionally, most adults with DS will eventually show both clinical and neuropathologic hallmarks of Alzheimer's disease (AD). The hippocampal formation constitutes the primary target for degeneration in both AD and DS. Over the past few years, we have studied the molecular mechanisms behind degeneration of this region and its major inputs in mouse models of DS. Our investigation has suggested that the loss of hippocampal inputs, particularly cholinergic and noradrenergic terminals, leads to de-afferentation of this region in the Ts65Dn mouse model of DS. Interestingly, we were able to link the overexpression of amyloid precursor protein (App) gene to degeneration of cholinergic and noradrenergic neurons in DS mouse models. We examined the underlying mechanisms of degeneration of multiple systems with extensive projections to the hippocampus in DS and its mouse models and the role of App overexpression in neurodegeneration. Understanding mechanisms behind hippocampal dysfunction has helped us to test several therapeutic strategies successfully in mouse models of DS. Here we review these strategies and mechanisms and discuss ways to translate our findings into possible interventions in humans.

    View details for DOI 10.1016/j.biopsych.2011.08.016

    View details for Web of Science ID 000300260700004

    View details for PubMedID 21945306

Conference Proceedings


  • BDNF Polymorphism Predicts the Rate of Decline in Skilled Task Performance and Hippocampal Volume in Healthy Individuals Das, D., Sanchez, M., Taylor, J., Noda, A., Yesavage, J., Salehi, A. LIPPINCOTT WILLIAMS & WILKINS. 2012

Presentations


  • The locus coeruleus - norepinephrine network optimizes coupling of cerebral blood volume with oxygen demand.

    Journal club discussing the role of norepinephrine in optimization of cerebral blood supply in response to oxygen demand

    Time Period

    12/29/2012

    Presented To

    WRIISC & MIRECC translational laboratory

    Location

    Palo Alto, CA

  • Improving Noradrenergic Signaling in the treatment of cognitive dysfunction in the Ts65Dn Mouse Model of Down Syndrome.

    Time Period

    10/2012

    Presented To

    Annual Meeting of Soceity for Neuroscience

    Location

    New Oleans, LA

  • Genetic Underpinnings of brain ventricular volume: Genome Wide Association Study (GWAS) and Meta-analysis.

    Time Period

    5/2012

    Presented To

    University of Texas Health Science Center at Houston

    Location

    Houston, TX

  • BDNF polymorphism predicts the rate of decline in skilled task performance and hippocampal volume.”

    Time Period

    4/2012

    Presented To

    American Association of Neurology

    Location

    New Orleans, LA

  • BDNF val66met Polymorphism: Associations with Longitudinal Flight Simulator Performance and Temporal Lobe Volume in Pilots over the Age of 40.

    Time Period

    4/2012

    Presented To

    Cognitive Aging Conference

    Location

    Atlanta, GA

  • Barriers to Obtaining Informed Consent in Acute Stroke Clinical Trials

    Time Period

    2/2012

    Presented To

    International Stroke Conference

    Location

    New Orleans, LA

  • The role of BDNF and its polymorphism in human cognitive functions.

    Time Period

    7/2010

    Presented To

    WRIISC & MIRECC translational laboratory

    Location

    Palo Alto, CA

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