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Wallerian Degeneration Slow mutation does not alter the amyloid pathology of Alzheimer's disease

  • Author(s): Shih, Ann Yu-Jung
  • et al.
Abstract

Wallerian Degeneration Slow (WLDs) has been found to have a neuroprotective role in many neuro-degenerative diseases, but never in the Alzheimer's disease models. Alzheimer's disease is the most common form of neurodegenerative disorder in the elderly afflicted with memory impairment and dementia. It is characterized by the deposition of amyloid beta-protein (A[Beta]) extracellularly within neuritic plaques and neurofibrillary tangles in neuronal cell bodies. It has been hypothesized that the deposition and aggregation of A[Beta] in the brain initiates a cascade of events, including synaptic dysfunction that results in AD. In this study, we crossed WLD animals with PDAPP, an APP over-expressing transgenic model, and found that WLD did not influence the survival rate, the level of amyloid beta or the amount of plaque deposit in the PDADD mice. However, we can not totally rule out the possibility that WLDs may have protective effects on APP transgenic models

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