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Katrin Andreasson

Professor of Neurology at Stanford University Medical Center

Katrin Andreasson is professor in the Department of Neurology and Neurological Sciences at Stanford University School of Medicine and is a physician-scientist with a longstanding commitment to understanding preclinical mechanisms leading to development of Alzheimer’s disease (AD). Dr. Andreasson cares for patients with dementia in the Stanford Memory Disorders Clinic, and carries out basic preclinical research in mouse models of neurodegeneration. A principal focus of Dr. Andreasson’s research has been the investigation of cellular and molecular mechanisms of brain injury mediated by cyclooxygenase and its downstream prostaglandin receptor pathways. The COX/PGE2 pathway has been implicated in brain injury in a broad spectrum of neurological diseases, including AD, where epidemiologic studies indicate a preventive effect of NSAIDs in cognitively normal aging human populations. Dr. Andreasson’s laboratory has identified harmful PGE2 receptors that contribute to AD-like pathology in AD model mice, and these findings are helping to drive efforts to develop antagonists to PGE2 receptors for prevention of AD. More recently, experiments modeling the preventive effects of NSAIDs in AD model mice have led to the hypothesis that increased tryptophan metabolism may contribute to early neuronal and later inflammatory pathology in AD.

Visit website: https://profiles.stanford.edu/katrin-andreasson

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See also: Academia Stanford University - Private research university, one of the world's leading research and teaching institutions

Details last updated 23-Jan-2021

Katrin Andreasson is also referenced in the following:

ARDD 2023 - 10th Aging Research & Drug Discovery Meeting

28-Aug-2023 to 01-Sep-2023

Event about latest progress in the molecular, cellular and organismal basis of aging organized by University of Copenhagen

Katrin Andreasson News

New evidence on reversing cognitive ageing in aged mice

The Scientist - 20-Jan-2021

EP2 receptor which causes inflammation & ageing was knocked down in a disease model

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