title: The Beta-amyloid protein of Alzheimer's disease: communication breakdown by modifying the neuronal cytoskeleton.
abstract: Alzheimer's disease (AD) is one of the most prevalent severe neurological disorders afflicting our aged population. Cognitive decline, a major symptom exhibited by AD patients, is associated with neuritic dystrophy, a degenerative growth state of neurites. The molecular mechanisms governing neuritic dystrophy remain unclear. Mounting evidence indicates that the AD-causative agent, β -amyloid protein (A β ), induces neuritic dystrophy. Indeed, neuritic dystrophy is commonly found decorating A β -rich amyloid plaques (APs) in the AD brain. Furthermore, disruption and degeneration of the neuronal microtubule system in neurons forming dystrophic neurites may occur as a consequence of A β -mediated downstream signaling. This review defines potential molecular pathways, which may be modulated subsequent to A β -dependent interactions with the neuronal membrane as a consequence of increasing amyloid burden in the brain.
authors.affiliation: Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC 3800, Australia.
authors.forename: Sara H
authors.initials: SH
authors.lastname: Mokhtar
authors.affiliation: Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC 3800, Australia.
authors.forename: Maha M
authors.initials: MM
authors.lastname: Bakhuraysah
authors.affiliation: Monash University, Clayton, VIC 3800, Australia.
authors.forename: David S
authors.initials: DS
authors.lastname: Cram
authors.affiliation: Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC 3800, Australia ; Department of Medicine, Central Clinical School, Monash University, Prahran, Clayton, VIC 3004, Australia.
authors.forename: Steven
authors.initials: S
authors.lastname: Petratos