School of Medicine


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  • Ahmad Salehi Najaf Abadi

    Ahmad Salehi Najaf Abadi

    Adjunct Professor, Psych/Public Mental Health & Population Sciences

    Bio Dr. Salehi is a neurobiologist working on identifying molecular mechanisms of neurodegenerative disorders including Alzheimer's disease and Down syndrome. In this process, ​he uses pre-clinical experiments to test the effects of already-approved drugs in improving cognitive function in the mouse models with hippocampal degeneration. In 2010, he received the World Technology Award for the innovative use of mouse models of Down syndrome to identify genes responsible for cognitive disabilities. Recently, he found that increasing beta2 adrenergic signaling would improve cognitive function in a mouse model of Down syndrome. Accordingly, in a collaborative study, he is testing whether already-approved beta2-adrenergic receptor agonists can indeed improve cognitive function and reduce the severity of pathology in individuals with mild to moderate Alzheimer’s disease.

    Selected Publications

    Dang V, Medina B, Das D, Moghadam S, Martin KJ, Lin B, Naik P, Patel D, Nosheny R, Wesson Ashford J, Salehi A. Formoterol, a long-acting β2 adrenergic agonist, improves cognitive function and promotes dendritic complexity in a mouse model of Down syndrome. Biol Psychiatry. 2014 Feb 1;75(3):179-88. doi: 10.1016/j.biopsych.2013.05.024. PMID: 23827853

    Salehi A, Faizi M, Colas D, Valletta J, Laguna J, Takimoto-Kimura R, Kleschevnikov A, Wagner SL, Aisen P, Shamloo M, Mobley WC. Restoration of norepinephrine-modulated contextual memory in a mouse model of Down syndrome. Sci Transl Med. 2009 Nov 18;1(7):7ra17. doi: 10.1126/scitranslmed.3000258.​ ​PMID: 20368182
    Salehi A, Delcroix JD, Belichenko PV, Zhan K, Wu C, Valletta JS, Takimoto-Kimura R, Kleschevnikov AM, Sambamurti K, Chung PP, Xia W, Villar A, Campbell WA, Kulnane LS, Nixon RA, Lamb BT, Epstein CJ, Stokin GB, Goldstein LS, Mobley WC. Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration. Neuron. 2006 Jul 6;51(1):29-42.​ ​PMID: 16815330

    Salehi A, Delcroix JD, Belichenko PV, Zhan K, Wu C, Valletta JS, Takimoto-Kimura R, Kleschevnikov AM, Sambamurti K, Chung PP, Xia W, Villar A, Campbell WA, Kulnane LS, Nixon RA, Lamb BT, Epstein CJ, Stokin GB, Goldstein LS, Mobley WC.Increased App expression in a mouse model of Down's syndrome disrupts NGF transport and causes cholinergic neuron degeneration.
    Neuron. 2006 Jul 6;51(1):29-42.

    Links:
    Lab: www.ahmadsalehi.info
    Linkedin: https://www.linkedin.com/in/ahmadsalehi1/
    Scholar: https://scholar.google.com/citations?user=Wr3FcsEAAAAJ&hl=en

  • Blake K. Scanlon, Ph.D.

    Blake K. Scanlon, Ph.D.

    Clinical Assistant Professor (Affiliated) [Vapahcs], Psych/Public Mental Health & Population Sciences

    Bio The overarching aim of Dr. Scanlon’s research is to develop and evaluate low-cost, pragmatic and clinically translatable methods for improving management of neurodegenerative disease and dementia. To that end, the Caregiver Technology Division of the Scanlon Lab aims to enhance patient- and family-centered care through novel, broadly customizable, and highly scalable caregiver interventions. In parallel, the Neurodegenerative Division of the Scanlon Lab focuses on the development and application of cognitive, neuropsychiatric, and biological markers for the initiation and progression of neurodegeneration.

    Dr. Scanlon received his bachelor’s degree in Neuroscience and doctorate in Clinical Health Psychology from the University of Miami. After concluding his clinical internship in Geropsychology/Neuropsychology at the VA Palo Alto Health Care System (VAPAHCS), he completed fellowships in Aging and Dementia at Stanford University School of Medicine and VAPAHCS. Dr. Scanlon is currently a VA Career Development Awardee in the Sierra-Pacific Mental Illness Research, Education, and Clinical Center (MIRECC) and Stanford/VA Aging Clinical Research Center where his work focuses on developing and evaluating low-cost, pragmatic and clinically translatable methods for improving management of neurodegenerative disease and dementia. He also serves as Co-Director of the Stanford/VA California Alzheimer's Disease Center, Chair of the VAPAHCS Dementia Committee, and Co-Chair of the Department of Veterans Affairs VISN 21 Dementia Committee.