Abstract:

Alzheimer’s disease (AD) is the most common cause of senile dementia. It is characterized by the formation of plaques mainly composed of the amyloid-beta peptide (Aβ). Diverse lines of evidence support the notion that accumulation of Aβ is a primary cause of AD pathogenesis. The current analyses suggest a model in which SorCS1 is not regulating Golgi-endosomal trafficking of APP, but is regulating its sorting and anterograde transport. Small alterations in APP trafficking may have a modest impact on Aβ generation, but probably result as a long-term effect over a lifetime in dramatic Aβ? accumulation. Therefore, understanding the intracellular sorting pathways of APP and its determinants in more detail will underlie the development of novel neuroprotective strategies.