Amyloid precursor protein (APP) is a key player in Alzheimer's disease (AD). The Aβ fragments of APP are the major constituent of AD-associated amyloid plaques, and mutations or duplications of the gene coding for APP can cause familial AD. Here we review the roles of APP in neuronal development, signaling, intracellular transport, and other aspects of neuronal homeostasis. We suggest that APP acts as a signaling nexus that transduces information about a range of extracellular conditions, including neuronal damage, to induction of intracellular signaling events. Subtle disruptions of APP signaling functions may be major contributors to AD-causing neuronal dysfunction.
|Number of pages||14|
|Publication status||Published - 23 Feb 2015|
- Amyloid beta-Protein Precursor/genetics
- Protein Processing, Post-Translational/genetics