Madhav Thambisetty

Summary

Affiliation: National Institutes of Health
Country: USA

Publications

  1. pmc Longitudinal changes in cortical thickness associated with normal aging
    Madhav Thambisetty
    Laboratory of Personality and Cognition, National Institute on Aging, Baltimore, MD 21224 2816, USA
    Neuroimage 52:1215-23. 2010
  2. pmc Blood-based biomarkers of Alzheimer's disease: challenging but feasible
    Madhav Thambisetty
    Laboratory of Personality and Cognition, Intramural Research Program, National Institue on Aging, NIH, USA
    Biomark Med 4:65-79. 2010
  3. pmc APOE epsilon4 genotype and longitudinal changes in cerebral blood flow in normal aging
    Madhav Thambisetty
    Department of Radiology and Radiological Sciences, Laboratory of Personality and Cognition, National Institute on Aging, National Institutes of Health, Johns Hopkins University, Baltimore, Maryland 21224 6825, USA
    Arch Neurol 67:93-8. 2010
  4. pmc Effect of complement CR1 on brain amyloid burden during aging and its modification by APOE genotype
    Madhav Thambisetty
    Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA
    Biol Psychiatry 73:422-8. 2013
  5. pmc Alzheimer risk variant CLU and brain function during aging
    Madhav Thambisetty
    Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA
    Biol Psychiatry 73:399-405. 2013
  6. doi request reprint Impaired glucose tolerance in midlife and longitudinal changes in brain function during aging
    Madhav Thambisetty
    Clinical and Translational Neuroscience Unit, Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Neurobiol Aging 34:2271-6. 2013
  7. pmc Baseline cardiovascular risk predicts subsequent changes in resting brain function
    Lori L Beason-Held
    Intramural Research Program, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA
    Stroke 43:1542-7. 2012
  8. pmc Proteome-based plasma markers of brain amyloid-β deposition in non-demented older individuals
    Madhav Thambisetty
    National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    J Alzheimers Dis 22:1099-109. 2010
  9. pmc Pharmacologic inhibition of ROCK2 suppresses amyloid-β production in an Alzheimer's disease mouse model
    Jeremy H Herskowitz
    Center for Neurodegenerative Disease, and Departments of Neurology, Cell Biology, and Biochemistry, Emory University School of Medicine, Atlanta, Georgia 30322, Medicinal Chemistry, Translational Research Institute, The Scripps Research Institute, Jupiter, Florida 33458, Department of Pathology, University of Washington, Seattle, Washington 98104, Departments of Pathology and Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, and Unit of Clinical and Translational Neuroscience and Laboratory of Behavioral Neuroscience, National Institute on Aging, Baltimore, Maryland 21224
    J Neurosci 33:19086-98. 2013
  10. pmc Plasma biomarkers of brain atrophy in Alzheimer's disease
    Madhav Thambisetty
    Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 6:e28527. 2011

Detail Information

Publications14

  1. pmc Longitudinal changes in cortical thickness associated with normal aging
    Madhav Thambisetty
    Laboratory of Personality and Cognition, National Institute on Aging, Baltimore, MD 21224 2816, USA
    Neuroimage 52:1215-23. 2010
    ..Significant nonlinear changes over time were observed in the postcentral, precentral, and orbitofrontal gyri on the left and inferior parietal, cingulate, and orbitofrontal gyri on the right...
  2. pmc Blood-based biomarkers of Alzheimer's disease: challenging but feasible
    Madhav Thambisetty
    Laboratory of Personality and Cognition, Intramural Research Program, National Institue on Aging, NIH, USA
    Biomark Med 4:65-79. 2010
    ....
  3. pmc APOE epsilon4 genotype and longitudinal changes in cerebral blood flow in normal aging
    Madhav Thambisetty
    Department of Radiology and Radiological Sciences, Laboratory of Personality and Cognition, National Institute on Aging, National Institutes of Health, Johns Hopkins University, Baltimore, Maryland 21224 6825, USA
    Arch Neurol 67:93-8. 2010
    ..Design, Setting, and..
  4. pmc Effect of complement CR1 on brain amyloid burden during aging and its modification by APOE genotype
    Madhav Thambisetty
    Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA
    Biol Psychiatry 73:422-8. 2013
    ..We examined the association between rs3818361 and brain amyloid deposition in nondemented older individuals...
  5. pmc Alzheimer risk variant CLU and brain function during aging
    Madhav Thambisetty
    Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA
    Biol Psychiatry 73:399-405. 2013
    ....
  6. doi request reprint Impaired glucose tolerance in midlife and longitudinal changes in brain function during aging
    Madhav Thambisetty
    Clinical and Translational Neuroscience Unit, Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Neurobiol Aging 34:2271-6. 2013
    ..Our findings suggest that IGT in midlife is associated with subsequent longitudinal changes in brain function during aging even in cognitively normal older individuals. ..
  7. pmc Baseline cardiovascular risk predicts subsequent changes in resting brain function
    Lori L Beason-Held
    Intramural Research Program, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA
    Stroke 43:1542-7. 2012
    ....
  8. pmc Proteome-based plasma markers of brain amyloid-β deposition in non-demented older individuals
    Madhav Thambisetty
    National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    J Alzheimers Dis 22:1099-109. 2010
    ..Our strategy combining proteomics with in vivo brain amyloid imaging holds promise for the discovery of biologically relevant peripheral markers in those at risk for AD...
  9. pmc Pharmacologic inhibition of ROCK2 suppresses amyloid-β production in an Alzheimer's disease mouse model
    Jeremy H Herskowitz
    Center for Neurodegenerative Disease, and Departments of Neurology, Cell Biology, and Biochemistry, Emory University School of Medicine, Atlanta, Georgia 30322, Medicinal Chemistry, Translational Research Institute, The Scripps Research Institute, Jupiter, Florida 33458, Department of Pathology, University of Washington, Seattle, Washington 98104, Departments of Pathology and Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland 21205, and Unit of Clinical and Translational Neuroscience and Laboratory of Behavioral Neuroscience, National Institute on Aging, Baltimore, Maryland 21224
    J Neurosci 33:19086-98. 2013
    ..Collectively, these findings highlight ROCK2 as a mechanism-based therapeutic target to combat Aβ production in AD. ..
  10. pmc Plasma biomarkers of brain atrophy in Alzheimer's disease
    Madhav Thambisetty
    Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
    PLoS ONE 6:e28527. 2011
    ..Moreover, these proteins are involved in complement activation and coagulation, providing further evidence for an intrinsic role of these pathways in AD pathogenesis...
  11. pmc Plasma clusterin concentration is associated with longitudinal brain atrophy in mild cognitive impairment
    Madhav Thambisetty
    Laboratory of Behavioral Neuroscience, National Institute on Aging, Baltimore, MD 21224, USA
    Neuroimage 59:212-7. 2012
    ..These findings in combination suggest an influence of this multi-functional protein on early stages of progression in AD pathology...
  12. pmc Alzheimer's disease risk genes and the age-at-onset phenotype
    Madhav Thambisetty
    Clinical and Translational Neuroscience Unit, Laboratory of Behavioral Neuroscience, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA
    Neurobiol Aging 34:2696.e1-5. 2013
    ..None of the other AD risk genes influenced AAO of AD. Our results suggest that besides APOE, other genes associated with AD risk do not exert large effects on the AAO phenotype of AD...
  13. pmc Abnormal gephyrin immunoreactivity associated with Alzheimer disease pathologic changes
    Chadwick M Hales
    From the Department of Neurology CMH, HR, AIL, JJL, TSW, Center for Neurodegenerative Disease CMH, HR, NTS, EBD, DMD, MG, AIL, JJL, TSW, Departments of Biochemistry NTS and Human Genetics EBD, TSW, and Pathology and Laboratory Medicine MG, Emory University School of Medicine, Atlanta, Georgia Department of Pathology, University of Washington, Seattle, Washington TJM Departments of Pathology and Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland JCT National Institute of Aging, National Institutes of Health, Bethesda, Maryland MT and Atlanta Veterans Administration Medical Center, Atlanta, Georgia TSW
    J Neuropathol Exp Neurol 72:1009-15. 2013
    ..Because gephyrin is involved in synaptic organization and synaptic dysfunction is an early event in AD, these findings point to its possible role in the pathogenesis of AD. ..
  14. pmc The utility of (11)C-arachidonate PET to study in vivo dopaminergic neurotransmission in humans
    Madhav Thambisetty
    Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bethesda, Maryland 20892, USA
    J Cereb Blood Flow Metab 32:676-84. 2012
    ..1-(11)C]AA PET may be useful for studying disturbances of dopaminergic neurotransmission in conditions such as Parkinson's disease and schizophrenia...