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Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
Published on: October 30, 2018
The Beta-amyloid protein of Alzheimer's disease: communication breakdown by modifying the neuronal cytoskeleton
Sara H Mokhtar1, Maha M Bakhuraysah1, David S Cram2
1Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC 3800, Australia.
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.
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