Affiliations: Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA | Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, MS, USA
Correspondence:
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Address for correspondence: Robert A. Rissman, Ph.D., Department of Neurosciences, UCSD School of Medicine, MTF 314, 9500 Gilman Drive, La Jolla, CA 92037-0624, USA. Tel.: +1 858 246 0140; Fax: +1 858 246 0139; E-mail: rrissman@ucsd.edu.
Abstract: Abnormally phosphorylated tau protein is a key component of the pathology seen in neurodegenerative tauopathies, such as Alzheimer's disease (AD). Despite its association with disease, tau phosphorylation (tau-P) also plays an important role in neuroplasticity, such as dendritic/synaptic remodeling seen in the hippocampus in response to environmental challenges, such as stress. To define the boundaries between neuroplasticity and neuropathology, studies have attempted to characterize the paradigms, stimuli, and signaling intermediates involved in stress-induced tau-P. Supporting an involvement of stress in AD are data demonstrating alterations in stress pathways and peptides in the AD brain and epidemiological data implicating stress exposure as a risk factor for AD. In this review, the question of whether stress-induced tau-P can be used as a model for examining the relationship between functional neuroplasticity and neuronal vulnerability will be discussed.
