APP Induces Neuronal Apoptosis Through APP-BP1-Mediated Downregulation of β-Catenin
Document Type
Short Survey
Publication Date
7-1-2004
Description
Alzheimer's disease (AD) is a neurodegenerative disease associated with progressive dementia. This mini-review focuses on how the amyloid precursor protein (APP) plays a central role in AD and Down syndrome as the regulator of the APP-BP1/hUba3 activated neddylation pathway. It is argued that the physiological function of APP is to downregulate the level of β-catenin. However, this APP function is abnormally amplified in patients with familial AD (FAD) mutations in APP and presenilins, resulting in the hyperactivation of neddylation and the decrease of β-catenin below a threshold level. Evidence in the literature is summarized to show that dysfunction of APP in downregulating β-catenin may underlie the mechanism of neuronal death in AD and Down syndrome.
Citation Information
Chen, Y. Z.. 2004. APP Induces Neuronal Apoptosis Through APP-BP1-Mediated Downregulation of β-Catenin. Apoptosis. Vol.9(4). 415-422. https://doi.org/10.1023/B:APPT.0000031447.05354.9f PMID: 15192323 ISSN: 1360-8185