Abstract
Lewy body disease (LBD) consists of Parkinson’s disease and dementia with Lewy bodies, and is pathologically characterized by the presence of cytoplasmic inclusions such as Lewy bodies. Formation of cytoplasmic inclusions is regarded as one of the pathophysiological events related to protein degradation systems – the ubiquitin–proteasome and autophagy–lysosome systems. Animal experiments clearly showed that alteration of these systems results in behavioral defects such as neurodegeneration and formation of ubiquitin-positive cytoplasmic inclusions. Our previous study has shown that autophagosomal components in LBD are qualitatively and quantitatively different from those in controls. These findings suggest that the autophagic process is impaired through alteration of autophagosomal components in LBD. Based on these results, we further discuss the capacity of autophagy to prevent LBD.
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