Gary E. Landreth, PhD
Martin Professor of Alzheimer's Research
Professor of Anatomy, Cell Biology & Physiology
Vice Director of Education, Stark Neurosciences Research Institute
- Phone
- (317) 278-7820
- Address
-
NB 214C
ANAT
IN
Indianapolis, IN - PubMed:
Bio
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.
| Year | Degree | Institution |
|---|---|---|
| 1977 | PhD | University of Michigan |
| 1972 | BA | University of Kansas |
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.
Desc: Zenith Society Fellow
Scope: National
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Desc: The Riuko and Archie Co Professor of Neurosciences
Scope: School
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Desc: Helen Ginsburg Award
Scope: State
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Desc: Paul Stark Lecturer
Scope: School
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Desc: Wells Lecturer
Scope: School
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Desc: Martin Chair in Alzheimer’s Disease Research
Scope: School
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