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, ß -amyloid protein (A ß ), induces neuritic dystrophy. Indeed, neuritic dystrophy is commonly found decorating A ß -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 ß -mediated downstream signaling. This review defines potential molecular pathways, which may be modulated subsequent to A ß -dependent interactions with the neuronal membrane as a consequence of increasing amyloid burden in the brain.