Abstract
The primal role that the amyloid-β (Aβ) peptide has in the development of Alzheimer's disease is now almost universally accepted. It is also well recognized that Aβ exists in multiple assembly states, which have different physiological or pathophysiological effects. Although the classical view is that Aβ is deposited extracellularly, emerging evidence from transgenic mice and human patients indicates that this peptide can also accumulate intraneuronally, which may contribute to disease progression.
Original language | English (US) |
---|---|
Pages (from-to) | 499-509 |
Number of pages | 11 |
Journal | Nature Reviews Neuroscience |
Volume | 8 |
Issue number | 7 |
DOIs | |
State | Published - Jul 2007 |
ASJC Scopus subject areas
- General Neuroscience