Gary E. Landreth

• Comment: Just resubmitting the same AI generated article even though you were asked not to is not good. Not disclosing you are a paid editor after being asked to is even worse. You clearly are WP:NOTHERE for any reason other than to advert your clients. No thanks. Sulfurboy (talk) 23:48, 1 August 2026 (UTC)

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Gary E. Landreth

Gary E. Landreth is an American neuroscientist whose research has focused on the molecular and cellular mechanisms underlying Alzheimer's disease, particularly the roles of microglia, neuroinflammation, apolipoprotein E (APOE), and innate immune signaling in disease pathogenesis. He is the Martin Chair in Alzheimer's Disease Research and Professor of Anatomy, Cell Biology & Physiology and Neurology at the Indiana University School of Medicine, where he also serves as Vice Director of Education at the Stark Neurosciences Research Institute....

Landreth is recognized for his contributions to understanding how the brain's innate immune system regulates Alzheimer's disease progression. His laboratory helped establish microglia as central mediators of neuroinflammation in Alzheimer's disease, identified mechanisms through which APOE promotes amyloid-β clearance, and demonstrated that activation of the nuclear receptors PPARγ, LXR, and RXR modulates microglial function and amyloid pathology. His work contributed to the clinical translation of nuclear receptor agonists, including PPARγ agonists and RXR agonists, as potential therapeutic approaches for Alzheimer's disease. In 2012, Landreth's research gained widespread attention after his laboratory reported that the FDA-approved cancer drug bexarotene rapidly cleared amyloid-β and improved cognitive deficits in mouse models of Alzheimer's disease. The findings were widely covered in the scientific and popular media and prompted early clinical studies evaluating the drug as a potential Alzheimer's therapy.

For more than two decades, Landreth's laboratory has investigated the mechanisms by which microglia-mediated neuroinflammation contributes to Alzheimer's disease. His group demonstrated that nuclear receptors and other immunometabolic pathways regulate microglial activation and inflammatory responses, providing a framework for therapeutic modulation of innate immunity in the brain. More recently, his laboratory has investigated the Alzheimer's disease risk genes TREM2 and PLCG2, examining how these genes regulate microglial phenotype, lipid metabolism, and innate immune responses during neurodegeneration.

Early life and education

Landreth received a Bachelor of Arts in Chemistry and Biochemistry from the University of Kansas in 1972. He earned a Ph.D. in Neuroscience from the University of Michigan in 1977, where he spent a year conducting research at the National Institute for Medical Research in London. He completed postdoctoral training in neurobiology at Stanford University under Eric M. Shooter in 1980.

Career

Landreth joined the faculty of the Medical University of South Carolina in 1980, where he was appointed Assistant Professor of Neurology and Anatomy. He was promoted to Associate Professor in 1986.

In 1989, Landreth joined Case Western Reserve University, where he established the Alzheimer's Research Laboratory and later became the Riuko and Archie Co Professor of Neurosciences. During his tenure, he directed the Alzheimer's Disease Research Center at University Hospitals Case Medical Center and led research on the molecular mechanisms of Alzheimer's disease and therapeutic development.

In 2017, Landreth joined the Indiana University School of Medicine as Professor of Anatomy, Cell Biology & Physiology and Neurology. He was appointed the Martin Chair in Alzheimer's Disease Research and became Vice Director of Education at the Stark Neurosciences Research Institute.

Honors and awards

• Zenith Society Fellow, Alzheimer's Association (2011–2014)
• Helen Ginsburg Award, Alzheimer's Association Colorado Chapter (2012)
• Paul Stark Lecturer, University of Rochester (2012)
• Riuko and Archie Co Professor of Neurosciences, Case Western Reserve University (2012–2017)
• Wells Lecturer, Michigan State University (2013)

• Martin Chair in Alzheimer's Disease Research, Indiana University School of Medicine (2017–present)

Select publications

• β-Amyloid stimulation of microglia and monocytes results in TNFα-dependent expression of inducible nitric oxide synthase and neuronal apoptosis. Combs et. al., J Neurosci. 2001 .
• Acute treatment with the PPARγ agonist pioglitazone and ibuprofen reduces glial inflammation and Aβ1–42 levels in APPV717I transgenic mice. Heneka et. al., Brain. 2005 .
• ApoE promotes the proteolytic degradation of Aβ. Jiang et.al., Neuron. 2008 .
• CD14 and toll-like receptors 2 and 4 are required for fibrillar Aβ-stimulated microglial activation. Reed-Geaghan et. al., J Neurosci. 2009 .
• The role of microglia in amyloid clearance from the AD brain. Lee et.al., J Neural Transm. 2010 .
• ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models. Cramer et. al., Science. 2012 .

• Neuroinflammation in Alzheimer's disease. Heneka et. al., Lancet Neurol. 2015 .
• Activation of the nuclear receptor PPARδ is neuroprotective in a transgenic mouse model of Alzheimer’s disease through inhibition of inflammation. Malm et.al., J Neuroinflammation. 2015

• TREM2 deficiency eliminates TREM2⁺ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models. Jay et. al., J Exp Med. 2015
• The niacin receptor HCAR2 modulates microglial response and limits disease progression in a mouse model of Alzheimer’s disease. Moutinho et. al., Sci Transl Med. 2022
• Genetic variants of phospholipase C-γ2 alter the phenotype and function of microglia and confer differential risk for Alzheimer’s disease. Tsai et. al., Immunity. 2023
• Therapeutic targeting of immunometabolism reveals a critical reliance on hexokinase 2 dosage for microglial activation and Alzheimer’s progression. Codocedo et. al., Cell Rep. 2024

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