The role of amyloid-beta in the regulation of memory.

Abstract

In this review there is evidence that amyloid-beta peptide is a memory enhancer at physiological (picomolar) concentrations. Pathological overproduction of amyloid-beta leads to impaired memory, oxidative damage, damage to the blood brain barrier, neurofibrillary tangles and amyloid plaque formation. Antisenses to amyloid precursor protein (APP) can reverse these effects in mice when they lower amyloid-beta protein to physiological levels. Data suggests that overproduction of APP leads to oxidative stress producing a vicious cycle of neuronal damage. For these reasons we have revised the "amyloid cascade hypothesis" removing emphasis from the plaque to amyloid-beta overproduction and suggest that an "amyloid-beta mitochondrial vicious cycle" hypothesis may be a better pathophysiological model for understanding Alzheimer's disease.

• Authors: John E Morley, Susan A Farr
• Journal: Biochemical pharmacology (Biochem Pharmacol) Vol. 88 Issue 4 Pg. 479-85 (Apr 15 2014) ISSN: 1873-2968 [Electronic] England
• PMID: 24398426 (Publication Type: Journal Article, Review)
• Copyright: Copyright © 2014 Elsevier Inc. All rights reserved.

Chemical References

• Amyloid beta-Peptides

Topics

• Amyloid beta-Peptides (biosynthesis, physiology)
• Animals
• Blood-Brain Barrier
• Memory (physiology)
• Mice
• Mitochondria (physiology)
• Plaque, Amyloid