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


  • Ahmad Salehi, Devsmita Das, Van Dang, Martha Millan Sanchez, Brian Medina. "United States Patent US 20140235726 Method 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.


All Publications

  • The Link Between Physical Activity and Cognitive Dysfunction in Alzheimer Disease PHYSICAL THERAPY Phillips, C., Baktir, M. A., Das, D., Lin, B., Salehi, A. 2015; 95 (7): 1046-1060


    Alzheimer disease (AD) is a primary cause of cognitive dysfunction in the elderly population worldwide. Despite the allocation of enormous amounts of funding and resources to studying this brain disorder, there are no effective pharmacological treatments for reducing the severity of pathology and restoring cognitive function in affected people. Recent reports on the failure of multiple clinical trials for AD have highlighted the need to diversify further the search for new therapeutic strategies for cognitive dysfunction. Thus, studies detailing the neuroprotective effects of physical activity (PA) on the brain in AD were reviewed, and mechanisms by which PA might mitigate AD-related cognitive decline were explored. A MEDLINE database search was used to generate a list of studies conducted between January 2007 and September 2014 (n=394). These studies, along with key references, were screened to identify those that assessed the effects of PA on AD-related biomarkers and cognitive function. The search was not limited on the basis of intensity, frequency, duration, or mode of activity. However, studies in which PA was combined with another intervention (eg, diet, pharmacotherapeutics, ovariectomy, cognitive training, behavioral therapy), and studies not written in English were excluded. Thirty-eight animal and human studies met entry criteria. Most of the studies suggested that PA attenuates neuropathology and positively affects cognitive function in AD. Although the literature lacked sufficient evidence to support precise PA guidelines, convergent evidence does suggest that the incorporation of regular PA into daily routines mitigates AD-related symptoms, especially when deployed earlier in the disease process. Here the protocols used to alter the progression of AD-related neuropathology and cognitive decline are highlighted, and the implications for physical therapist practice are discussed.

    View details for DOI 10.2522/ptj.20140212

    View details for Web of Science ID 000357236800010

    View details for PubMedID 25573757

  • Assessment of dendritic arborization in the dentate gyrus of the hippocampal region in mice. Journal of visualized experiments : JoVE Das, D., Phillips, C., Lin, B., Mojabi, F., Akif Baktir, M., Dang, V., Ponnusamy, R., Salehi, A. 2015


    Dendritic arborization has been shown to be a reliable marker for examination of structural and functional integrity of neurons. Indeed, the complexity and extent of dendritic arborization correlates well with the synaptic plasticity in these cells. A reliable method for assessment of dendritic arborization is needed to characterize the deleterious effects of neurological disorders on these structures and to determine the effects of therapeutic interventions. However, quantification of these structures has proven to be a formidable task given their complex and dynamic nature. Fortunately, sophisticated imaging techniques can be paired with conventional staining methods to assess the state of dendritic arborization, providing a more reliable and expeditious means of assessment. Below is an example of how these imaging techniques were paired with staining methods to characterize the dendritic arborization in wild type mice. These complementary imaging methods can be used to qualitatively and quantitatively assess dendritic arborization that span a rather wide area within the hippocampal region.

    View details for DOI 10.3791/52371

    View details for PubMedID 25867799

  • Nest building is impaired in the Ts65Dn mouse model of Down syndrome and rescued by blocking 5HT2a receptors NEUROBIOLOGY OF LEARNING AND MEMORY Heller, H. C., Salehi, A., Chuluun, B., Das, D., Lin, B., Moghadam, S., Garner, C. C., Colas, D. 2014; 116: 162-171


    Down syndrome (DS) has an incidence of about 1/700 births, and is therefore the most common cause of cognitive and behavioral impairments in children. Recent studies on mouse models of DS indicate that a number of pharmacotherapies could be beneficial for restoring cognitive abilities in individuals with DS. Attention deficits that are present in DS account in part for learning and memory deficiencies yet have been scarcely studied in corresponding models. Investigations of this relevant group of behaviors is more difficult in mouse models because of the difficulty in homologizing mouse and human behaviors and because standard laboratory environments do not always elicit behaviors of interest. Here we characterize nest building as a goal-directed behavior that is seriously impaired in young Ts65Dn mice, a genetic model of DS. We believe this impairment may reflect in part attention deficits, and we investigate the physiological, genetic, and pharmacological factors influencing its expression. Nesting behavior in young Ts65Dn mice was severely impaired when the animals were placed in a novel environment. But this context-dependent impairment was transient and reversible. The genetic determinants of this deficiency are restricted to a ∼100 gene segment on the murine chromosome 16. Nest building behavior is a highly integrated phenotypic trait that relies in part on limbic circuitry and on the frontal cortex in relation to cognitive and attention processes. We show that both serotonin content and 5HT2a receptors are increased in the frontal cortex of Ts65Dn mice and that pharmacological blockage of 5HT2a receptors in Ts65Dn mice rescues their context dependent nest building impairment. We propose that the nest-building trait could represent a marker of attention related deficits in DS models and could be of value in designing pharmacotherapies for this specific aspect of DS. 5HT2a modulation may improve goal-directed behavior in DS.

    View details for DOI 10.1016/j.nlm.2014.10.002

    View details for Web of Science ID 000346393800018

  • The role of NMDA receptors in the pathophysiology and treatment of mood disorders NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS Ghasemi, M., Phillips, C., Trillo, L., De Miguel, Z., Das, D., Salehi, A. 2014; 47: 336-358


    Mood disorders such as major depressive disorder and bipolar disorder are chronic and recurrent illnesses that cause significant disability and affect approximately 350 million people worldwide. Currently available biogenic amine treatments provide relief for many and yet fail to ameliorate symptoms for others, highlighting the need to diversify the search for new therapeutic strategies. Here we present recent evidence implicating the role of N-methyl-D-aspartate receptor (NMDAR) signaling in the pathophysiology of mood disorders. The possible role of NMDARs in mood disorders has been supported by evidence demonstrating that: (i) both BPD and MDD are characterized by altered levels of central excitatory neurotransmitters; (ii) NMDAR expression, distribution, and function are atypical in patients with mood disorders; (iii) NMDAR modulators show positive therapeutic effects in BPD and MDD patients; and (iv) conventional antidepressants/mood stabilizers can modulate NMDAR function. Taken together, this evidence suggests the NMDAR system holds considerable promise as a therapeutic target for developing next generation drugs that may provide more rapid onset relief of symptoms. Identifying the subcircuits involved in mood and elucidating the role of NMDARs subtypes in specific brain circuits would constitute an important step toward the development of more effective therapies with fewer side effects.

    View details for DOI 10.1016/j.neubiorev.2014.08.017

    View details for Web of Science ID 000347498900022

    View details for PubMedID 25218759

  • Neurotransmitter-based strategies for the treatment of cognitive dysfunction in Down syndrome PROGRESS IN NEURO-PSYCHOPHARMACOLOGY & BIOLOGICAL PSYCHIATRY Das, D., Phillips, C., Hsieh, W., Sumanth, K., Van Dang, V., Salehi, A. 2014; 54: 140-148
  • Formoterol, a Long-Acting beta 2 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., Martin, K. J., Lin, B., Naik, P., Patel, D., Nosheny, R., Ashford, J. W., Salehi, A. 2014; 75 (3): 179-188
  • Ascending monoaminergic systems alterations in Alzheimer's disease. Translating basic science into clinical care NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS Trillo, L., Das, D., Hsieh, W., Medina, B., Moghadam, S., Lin, B., Dang, V., Sanchez, M. M., De Miguel, Z., Ashford, J. W., Salehi, A. 2013; 37 (8): 1363-1379


    Extensive neuropathological studies have established a compelling link between abnormalities in structure and function of subcortical monoaminergic (MA-ergic) systems and the pathophysiology of Alzheimer's disease (AD). The main cell populations of these systems including the locus coeruleus, the raphe nuclei, and the tuberomamillary nucleus undergo significant degeneration in AD, thereby depriving the hippocampal and cortical neurons from their critical modulatory influence. These studies have been complemented by genome wide association studies linking polymorphisms in key genes involved in the MA-ergic systems and particular behavioral abnormalities in AD. Importantly, several recent studies have shown that improvement of the MA-ergic systems can both restore cognitive function and reduce AD-related pathology in animal models of neurodegeneration. This review aims to explore the link between abnormalities in the MA-ergic systems and AD symptomatology as well as the therapeutic strategies targeting these systems. Furthermore, we will examine possible mechanisms behind basic vulnerability of MA-ergic neurons in AD.

    View details for DOI 10.1016/j.neubiorev.2013.05.008

    View details for Web of Science ID 000326902600005

    View details for PubMedID 23707776

  • 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


    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

  • BDNF polymorphism predicts the rate of decline in skilled task performance and hippocampal volume in healthy individuals TRANSLATIONAL PSYCHIATRY Sanchez, M. M., Das, D., Taylor, J. L., Noda, A., Yesavage, J. A., Salehi, A. 2011; 1


    Numerous studies have indicated a link between the presence of polymorphism in brain-derived neurotrophic factor (BDNF) and cognitive and affective disorders. However, only a few have studied these effects longitudinally along with structural changes in the brain. This study was carried out to investigate whether valine-to-methionine substitution at position 66 (val66met) of pro-BDNF could be linked to alterations in the rate of decline in skilled task performance and structural changes in hippocampal volume. Participants consisted of 144 healthy Caucasian pilots (aged 40-69 years) who completed a minimum of 3 consecutive annual visits. Standardized flight simulator score (SFSS) was measured as a reliable and quantifiable indicator for skilled task performance. In addition, a subset of these individuals was assessed for hippocampal volume alterations using magnetic resonance imaging. We found that val66met substitution in BDNF correlated longitudinally with the rate of decline in SFSS. Structurally, age-dependent hippocampal volume changes were also significantly altered by this substitution. Our study suggests that val66met polymorphism in BDNF can be linked to the rate of decline in skilled task performance. Furthermore, this polymorphism could be used as a predictor of the effects of age on the structure of the hippocampus in healthy individuals. Such results have implications for understanding possible disabilities in older adults performing skilled tasks who are at a higher risk for cognitive and affective disorders.Translational Psychiatry (2011) 1, e51; doi:10.1038/tp.2011.47; published online 25 October 2011.

    View details for DOI 10.1038/tp.2011.47

    View details for Web of Science ID 000306216300008

    View details for PubMedID 22833197