The Beta-Amyloid Protein of Alzheimer’s Disease : Communication Breakdown by Modifying the Neuronal Cytoskeleton

Abstract EN

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 (Aβ), induces neuritic dystrophy.

Indeed, neuritic dystrophy is commonly found decorating Aβ-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 Aβ-mediated downstream signaling.

This review defines potential molecular pathways, which may be modulated subsequent to Aβ-dependent interactions with the neuronal membrane as a consequence of increasing amyloid burden in the brain.