Affiliations: Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, MS, USA | Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson, MS, USA
Correspondence:
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Address for correspondence: Garth Bissette, Ph.D., Department of Psychiatry and Human Behavior, 720 James H. Hardy Clinical Sciences Building, University of Mississippi Medical Center, 2500 North State Street, Jackson, MS 39216-4505, USA. Tel.: +1 601 984 6683; Fax: +1 601 984 5885; E-mail: gbissette@psychiatry.umsmed.edu.
Abstract: This review explores the data indicating that the initial production of amyloid-β precursor protein and phosphorylated tau are associated with physiological mechanisms for repair or protection of neurons exposed to significant disturbances in homeostasis. Stimuli as diverse as head injury, inhaled anesthetic agents, stimulant drugs, and both physiological (restraint) and psychological stress (social isolation) have been shown to increase brain expression of amyloid-β and hyperphosphorylated tau without accompanying neurodegeneration. This review aims to encompass these responses as indicators of normal physiological processes that, in the case of Alzheimer's disease, are either unable to successfully repair or protect vulnerable neuronal populations from eventual neurodegeneration, but that are necessary components of an integrated nervous system that would be more susceptible to pathology if such processes were blocked in an attempt to minimize or prevent future damage.
