Functional Impact of Corticotropin-Releasing Factor Exposure on Tau Phosphorylation and Axon Transport

PloS One
Michelle H LeRobert A Rissman

Abstract

Stress exposure or increased levels of corticotropin-releasing factor (CRF) induce hippocampal tau phosphorylation (tau-P) in rodent models, a process that is dependent on the type-1 CRF receptor (CRFR1). Although these preclinical studies on stress-induced tau-P provide mechanistic insight for epidemiological work that identifies stress as a risk factor for Alzheimer's disease (AD), the actual impact of stress-induced tau-P on neuronal function remains unclear. To determine the functional consequences of stress-induced tau-P, we developed a novel mouse neuronal cell culture system to explore the impact of acute (0.5hr) and chronic (2hr) CRF treatment on tau-P and integral cell processes such as axon transport. Consistent with in vivo reports, we found that chronic CRF treatment increased tau-P levels and caused globular accumulations of phosphorylated tau in dendritic and axonal processes. Furthermore, while both acute and chronic CRF treatment led to significant reduction in CREB activation and axon transport of brain-derived neurotrophic factor (BDNF), this was not the case with mitochondrial transport. Acute CRF treatment caused increased mitochondrial velocity and distance traveled in neurons, while chronic CRF treatment m...Continue Reading

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Jun 22, 2017·Molecular Neurodegeneration·Hunter S FutchTodd E Golde
Jul 13, 2017·Cellular and Molecular Neurobiology·Boris MravecAlexandra Padova
Sep 26, 2019·Frontiers in Pharmacology·Alessandra CarusoSergio Scaccianoce
May 18, 2020·Pharmacological Research : the Official Journal of the Italian Pharmacological Society·Clément BarbereauMireille Rossel

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