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Eliezer Masliah

Researcher Next ID · RN-022520

Researcher · Medicine

National Institutes of Health

Bethesda, United States

Not currently recruitingFunding unknown
Works count
1,235
Citation count
182,349
H-index
195
i10-index
902

Research interests

Medicine
Neuroscience
Immunology and Microbiology
Alzheimer's disease research and treatments
Parkinson's Disease Mechanisms and Treatments
Neuroinflammation and Neurodegeneration Mechanisms
HIV Research and Treatment
Nuclear Receptors and Signaling

Publications

  • Anatomically interpretable deep learning of brain age captures domain-specific cognitive impairment

    Proceedings of the National Academy of Sciences · 2023 · https://doi.org/10.1073/pnas.2214634120

  • Genome sequencing analysis identifies new loci associated with Lewy body dementia and provides insights into its genetic architecture

    Nature Genetics · 2021 · https://doi.org/10.1038/s41588-021-00785-3

  • A nonsynonymous mutation in PLCG2 reduces the risk of Alzheimer’s disease, dementia with Lewy bodies and frontotemporal dementia, and increases the likelihood of longevity

    Acta Neuropathologica · 2019 · https://doi.org/10.1007/s00401-019-02026-8

  • NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease

    Alzheimer s & Dementia · 2018 · https://doi.org/10.1016/j.jalz.2018.02.018

  • Diagnosis and management of dementia with Lewy bodies

    Neurology · 2017 · https://doi.org/10.1212/wnl.0000000000004058

  • Investigating the genetic architecture of dementia with Lewy bodies: a two-stage genome-wide association study

    The Lancet Neurology · 2017 · https://doi.org/10.1016/s1474-4422(17)30400-3

  • Defective synaptic connectivity and axonal neuropathology in a human iPSC-based model of familial Parkinson’s disease

    Proceedings of the National Academy of Sciences · 2017 · https://doi.org/10.1073/pnas.1617259114

  • Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium

    Carolina Digital Repository (University of North Carolina at Chapel Hill) · 2017 · https://doi.org/10.17615/8xge-z676

  • Autophagy inhibition promotes SNCA/alpha-synuclein release and transfer via extracellular vesicles with a hybrid autophagosome-exosome-like phenotype

    Autophagy · 2017 · https://doi.org/10.1080/15548627.2017.1395992

  • PART, a distinct tauopathy, different from classical sporadic Alzheimer disease

    Acta Neuropathologica · 2015 · https://doi.org/10.1007/s00401-015-1407-2

  • Primary age-related tauopathy (PART): a common pathology associated with human aging

    Acta Neuropathologica · 2014 · https://doi.org/10.1007/s00401-014-1349-0

  • TMEM106B is a genetic modifier of frontotemporal lobar degeneration with C9orf72 hexanucleotide repeat expansions

    Acta Neuropathologica · 2014 · https://doi.org/10.1007/s00401-013-1239-x

  • The many faces of α-synuclein: from structure and toxicity to therapeutic target

    Nature reviews. Neuroscience · 2012 · https://doi.org/10.1038/nrn3406

  • Inhibitory Interneuron Deficit Links Altered Network Activity and Cognitive Dysfunction in Alzheimer Model

    Cell · 2012 · 10.1016/j.cell.2012.02.046

  • Evidence for a role of the rare p.A152T variant in MAPT in increasing the risk for FTD-spectrum and Alzheimer's diseases

    Human Molecular Genetics · 2012 · https://doi.org/10.1093/hmg/dds161

  • National Institute on Aging–Alzheimer's Association guidelines for the neuropathologic assessment of Alzheimer's disease

    Alzheimer s & Dementia · 2012 · 10.1016/j.jalz.2011.10.007

  • Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature

    Journal of Neuropathology & Experimental Neurology · 2012 · https://doi.org/10.1097/nen.0b013e31825018f7

  • National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach

    Acta Neuropathologica · 2011 · 10.1007/s00401-011-0910-3

  • Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease

    Nature Genetics · 2011 · 10.1038/ng.801

  • In vivo demonstration that α-synuclein oligomers are toxic

    Proceedings of the National Academy of Sciences · 2011 · 10.1073/pnas.1100976108

  • Neuropathological Alterations in Alzheimer Disease

    Cold Spring Harbor Perspectives in Medicine · 2011 · https://doi.org/10.1101/cshperspect.a006189

  • Common variants at 7p21 are associated with frontotemporal lobar degeneration with TDP-43 inclusions

    Nature Genetics · 2010 · 10.1038/ng.536

  • Polyamine pathway contributes to the pathogenesis of Parkinson disease

    Proceedings of the National Academy of Sciences · 2010 · https://doi.org/10.1073/pnas.1011751107

  • Transsynaptic Progression of Amyloid-β-Induced Neuronal Dysfunction within the Entorhinal-Hippocampal Network

    Neuron · 2010 · https://doi.org/10.1016/j.neuron.2010.10.020

  • Inclusion formation and neuronal cell death through neuron-to-neuron transmission of α-synuclein

    Proceedings of the National Academy of Sciences · 2009 · 10.1073/pnas.0903691106

  • Ubiquitinated TDP-43 in Frontotemporal Lobar Degeneration and Amyotrophic Lateral Sclerosis

    Science · 2006 · https://doi.org/10.1126/science.1134108

  • Axonopathy and Transport Deficits Early in the Pathogenesis of Alzheimer's Disease

    Science · 2005 · 10.1126/science.1105681

  • α-Synuclein is phosphorylated in synucleinopathy lesions

    Nature Cell Biology · 2002 · 10.1038/ncb748

  • High-Level Neuronal Expression of Aβ1–42in Wild-Type Human Amyloid Protein Precursor Transgenic Mice: Synaptotoxicity without Plaque Formation

    Journal of Neuroscience · 2000 · 10.1523/jneurosci.20-11-04050.2000

  • Dopaminergic Loss and Inclusion Body Formation in α-Synuclein Mice: Implications for Neurodegenerative Disorders

    Science · 2000 · 10.1126/science.287.5456.1265

  • Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein

    Nature · 1995 · 10.1038/373523a0

  • The precursor protein of non-Aβ component of Alzheimer's disease amyloid is a presynaptic protein of the central nervous system

    Neuron · 1995 · 10.1016/0896-6273(95)90302-x

  • Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease.

    Proceedings of the National Academy of Sciences · 1993 · 10.1073/pnas.90.23.11282

  • Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment

    Annals of Neurology · 1991 · https://doi.org/10.1002/ana.410300410

Current projects

    No projects listed.