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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.

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