Does Alzheimer's Disease Result from Attempts at Repair or Protection After Transient Stress?

摘要: This review explores the data indicating that initial production of amyloid-beta precursor protein and phosphorylated tau are associated with physiological mechanisms for repair or protection neurons exposed to significant disturbances in homeostasis. Stimuli as diverse head injury, inhaled anesthetic agents, stimulant drugs, both (restraint) psychological stress (social isolation) have been shown increase brain expression hyperphosphorylated without accompanying neurodegeneration. aims encompass these responses indicators normal processes that, case Alzheimer's disease, either unable successfully protect vulnerable neuronal populations from eventual neurodegeneration, but necessary components an integrated nervous system would be more susceptible pathology if such were blocked attempt minimize prevent future damage.