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NotificationsNotify me of updates to ENDOCYTIC DYSFUNCTYION AND ALZHEIMER’S DISEASE pp. 223-230
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Authors:  Nobuyuki Kimura, Laboratory of Disease Control, Tsukuba Primate Research Center, National Institute of Biomedical Innovation, Ibaraki, Japan
Although the extracellular deposition of  -amyloid protein (A) as senile plaques (SPs) is an invariable pathological feature of Alzheimer's disease (AD), recent studies suggest that the accumulation of intracellular Amay represent an early event in the pathogenesis of AD. In the case of familial AD, evidently the expression of causative genetic mutations likely enhances Ageneration, which can cause buildup of intracellular A. However, how intracellular Aaccumulates in sporadic AD, a major form of the disease, remains to be clarified.
Recently, growing evidences suggest that endocytic dysfunction is involved in AD pathology. In brains of early stage AD patients, neuronal endocytic pathology such as the accumulation of -amyloid precursor protein (APP) in enlarged early endosomes is observed even before SP deposition. Moreover, endocytic dysfunction induces Aaccumulation in endosomal compartments. Ais produced from APP through sequential proteolytic cleavages by - and -secreatases, and such amyloidogenic cleavage of APP can occur through the endocytic pathway. These findings suggest that endocytosis is involved in APP metabolism itself and that endocytic dysfunction may cause the accumulation of intracellular A. In this review, I summarize findings at present and discuss the hypothesis that endocytic dysfunction may underlie AD pathology. 

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