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Gregory Cole

· Professor in Residence

University of California, Los Angeles · Geriatrics and Gerontology

Active 1985–2022

h-index87
Citations49.7k
Papers2302 last 5y
Funding$69.7M

Academic metrics are sourced from OpenAlex and public funding records; values may differ from Google Scholar.

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About

Gregory M. Cole is a Professor-in-Residence in the Department of Neurology at UCLA's David Geffen School of Medicine. His research primarily focuses on neurodegenerative diseases, particularly Alzheimer's disease, exploring mechanisms of pathology and potential therapeutic interventions. His work includes investigating tauopathy in mice and humans, surrogate plasma biomarkers for brain trauma-initiated neurodegenerative disease, and modulating innate immune function to prevent age-related neurodegeneration. Dr. Cole has contributed significantly to understanding the biochemical and molecular underpinnings of Alzheimer's, including amyloid pathology, synaptic biomarkers, and neuroinflammation. His research employs a multidisciplinary approach, integrating pharmacogenomics, multiomics analysis, and innovative imaging techniques to identify biomarkers and develop potential treatments for neurodegenerative conditions.

Research topics

  • Biochemistry
  • Chemistry
  • Chromatography
  • Psychology
  • Genetics
  • Medicine
  • Clinical psychology
  • Biology
  • Bioinformatics
  • Internal medicine

Selected publications

  • Neuroinflammation in Alzheimer's disease

    The Lancet Neurology · 2015-03-16 · 6026 citations

    reviewOpen access
  • Oral curcumin for Alzheimer's disease: tolerability and efficacy in a 24-week randomized, double blind, placebo-controlled study

    Alzheimer s Research & Therapy · 2012-10-29 · 522 citations

    articleOpen accessSenior author

    INTRODUCTION: Curcumin is a polyphenolic compound derived from the plant Curcuma Long Lin that has been demonstrated to have antioxidant and anti-inflammatory effects as well as effects on reducing beta-amyloid aggregation. It reduces pathology in transgenic models of Alzheimer's disease (AD) and is a promising candidate for treating human AD. The purpose of the current study is to generate tolerability and preliminary clinical and biomarker efficacy data on curcumin in persons with AD. METHODS:…

  • Curcumin Suppresses Soluble Tau Dimers and Corrects Molecular Chaperone, Synaptic, and Behavioral Deficits in Aged Human Tau Transgenic Mice

    Journal of Biological Chemistry · 2012-12-23 · 207 citations

    articleOpen access

    The mechanisms underlying Tau-related synaptic and cognitive deficits and the interrelationships between Tau species, their clearance pathways, and synaptic impairments remain poorly understood. To gain insight into these mechanisms, we examined these interrelationships in aged non-mutant genomic human Tau mice, with established Tau pathology and neuron loss. We also examined how these interrelationships changed with an intervention by feeding mice either a control diet or one containing the bra…

  • Clinical development of curcumin in neurodegenerative disease

    Expert Review of Neurotherapeutics · 2015-06-02 · 177 citations

    reviewOpen access

    Curcumin, a polyphenolic antioxidant derived from the turmeric root has undergone extensive preclinical development, showing remarkable efficacy in wound repair, cancer and inflammatory disorders. This review addresses the rationale for its use in neurodegenerative disease, particularly Alzheimer’s disease (AD). Curcumin is a pleiotropic molecule, which not only directly binds to and limits aggregation of the β-sheet conformations of amyloid characteristic of many neurodegenerative diseases but…

  • Loss of MAP Function Leads to Hippocampal Synapse Loss and Deficits in the Morris Water Maze with Aging

    Journal of Neuroscience · 2014-05-21 · 134 citations

    articleOpen accessSenior author

    Hyperphosphorylation and accumulation of tau aggregates are prominent features in tauopathies, including Alzheimer's disease, but the impact of loss of tau function on synaptic and cognitive deficits remains poorly understood. We report that old (19-20 months; OKO) but not middle-aged (8-9 months; MKO) tau knock-out mice develop Morris Water Maze (MWM) deficits and loss of hippocampal acetylated α-tubulin and excitatory synaptic proteins. Mild motor deficits and reduction in tyrosine hydroxylase…

Recent grants

Frequent coauthors

Education

  • M.D.

    University of California, Los Angeles

  • B.A.

    University of California, Los Angeles

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