Abstract
Familial Alzheimer's disease mutations in presenilin and the amyloid precursor protein (APP) are thought to cause Alzheimer's disease (AD) neurodegeneration by increasing production and aggregation of amyloid beta (Aβ). However, presenilin has functions that are distinct from its role in the γ-secretase complex, while APP has signaling functions that transcend its role as the source of Aβ. Three recent papers highlight the potential importance of presenilin and APP signaling in the etiology of AD.
Abbreviations | ||
APP | = | amyloid precursor protein; |
FAD | = | familial Alzheimer's disease; |
PI3K | = | phosphatidylinositol-3-kinase; |
GSK-3 | = | glycogen synthase kinase 3; |
EGFR | = | epidermal growth factor receptor |
Abbreviations | ||
APP | = | amyloid precursor protein; |
FAD | = | familial Alzheimer's disease; |
PI3K | = | phosphatidylinositol-3-kinase; |
GSK-3 | = | glycogen synthase kinase 3; |
EGFR | = | epidermal growth factor receptor |