27243-Landreth, Gary

Gary E. Landreth, PhD

Martin Professor of Alzheimer's Research

NB 214C
Indianapolis, IN
Pubmed Logo


Dr. Landreth received his undergraduate degree in Chemistry and Biochemistry from the University of Kansas in 1972.  He then completed a Ph.D. in the Neuroscience Program at the University of Michigan, including a year of study at the National Institute of Medical Research in London.  He carried out postdoctoral work in the Department of Neurobiology at Stanford with Dr. Eric Shooter. Dr. Landreth was appointed to the faculty of the Medical University of South Carolina in 1980, where he worked for 9 years. He moved to Case Western Reserve University Department of Neurosciences and directed the Alzheimer Research Laboratory from 1989 until 2016. He is presently on the faculty of the University of Indiana School of Medicine and Stark Neurosciences Research Institute.

Dr. Landreth’s work over the past 20 years has focused the principal genetic risk factors for Alzheimer’s disease. The laboratory has focused on the biology of ApoE, its role in amyloid homeostasis and the regulation of its expression by nuclear receptors. The laboratory has also investigated inflammatory mechanisms in Alzheimer’s disease and the biology of microglia.  Recent work has examined the mechanisms through which TREM2 influences disease pathogenesis. The laboratory maintains a focus on drug development for CNS disorders, including Alzheimer’s disease.

Titles & Appointments

  • Martin Professor of Alzheimer's Research
  • Professor of Anatomy, Cell Biology & Physiology
  • Vice Director of Education, Stark Neurosciences Research Institute
  • Education
    1977 PhD University of Michigan
    1972 BA University of Kansas
  • Research

    The Landreth lab investigates the roles of genetic risk factors in Alzheimer’s disease pathogenesis and employs state of the art genetic models to dissect the underlying disease mechanisms.

    Alzheimer’s disease is accompanied by a robust inflammatory response mediated by the brain’s resident macrophages, or microglia. Recent GWAS studies have demonstrated that about 40% of all AD risk genes are linked to this immune response. We are investigating the microglial gene, TREM2, which confers greatly elevated risk for the disease. Similarly, genetic variants of the intracellular signaling protein, PLCg2, confers both elevated risk for AD, but can also confer protection from disease and we are investigating how this gene operates in microglia to regulate the immune response.

    Alzheimer’s disease is typified by altered energy metabolism. We are exploring how the microglia act to alter brain metabolism. We are examining how disease affects microglia glucose utilization and gene expression and, in turn, how these cells influence neuronal activity and metabolism. We have an active research program examining the therapeutic utility of nuclear receptor agonists which act through pleiotropic mechanisms to regulate both cellular metabolism and microglial inflammation.  

  • Awards
    Org: Alzheimer’s Association
    Desc: Zenith Society Fellow
    Scope: National
    Org: Case Western Reserve University
    Desc: The Riuko and Archie Co Professor of Neurosciences
    Scope: School
    Org: Alzheimer’s Association Colorado Chapter
    Desc: Helen Ginsburg Award
    Scope: State
    Org: University of Rochester
    Desc: Paul Stark Lecturer
    Scope: School
    Org: Michigan State University
    Desc: Wells Lecturer
    Scope: School
    Org: Indiana University
    Desc: Martin Chair in Alzheimer’s Disease Research
    Scope: School

Research Labs

Faculty research at IU School of Medicine is transforming health. Details about the medical research being conducted in faculty labs throughout IU School of Medicine are available in the Research section of this site.

Faculty Labs