Selective suppression of the α isoform of p38 MAPK rescues late-stage tau pathology

Abstract

Hyperphosphorylation and aggregation of tau protein are the pathological hallmarks of Alzheimer’s disease and related tauopathies. We previously demonstrated that the microglial activation induces tau hyperphosphorylation and cognitive impairment via activation of p38 mitogen-activated protein kinase (p38 MAPK) in the hTau mouse model of tauopathy that was deficient for microglial fractalkine receptor CX3CR1.

Document Details

• Document Type: Pub Defense Publication
• Publication Date: Dec 01, 2016
• Source ID: 10.1186/s13195-016-0221-y

Entities

People

• Bruce T. Lamb
• D. Martin Watterson
• Guixiang Xu
• Kiran Bhaskar
• Linda J. Van Eldik
• Nicole Maphis
• Olga N. Kokiko-cochran
• Saktimayee M. Roy
• Shanya Jiang

Organizations

• Alzheimer's Association
• BrightFocus Foundation
• National Institute of Neurological Disorders and Stroke
• National Institute on Aging
• United States Department of Defense

Tags

Fields of Study

• Biology

Readers

• Cellular and Molecular Pathways of Apoptosis.
• Traumatic Brain Injury (TBI) and Cognitive Aging in the Guam and Border Populations Affected by Alzheimer's Disease and Tau-Associated Dementias.