Abnormal accumulation of NACP/alpha-synuclein in neurodegenerative disorders

摘要: The precursor of the non-Abeta component Alzheimer's disease amyloid (NACP) (also known as a-synuclein) is a presynaptic terminal molecule that accumulates in plaques disease. Recent studies have shown mutation NACP associated with familial Parkinson's disease, and Lewy bodies are immunoreactive antibodies against this molecule. To clarify patterns accumulation differences abnormal compartmentalization, we studied immunoreactivity using double immunolabeling laser scanning confocal microscopy cortex patients various neurodegenerative disorders. In body variant diffuse was found to immunolabel cortical bodies, neurites, dystrophic neurites plaques. Double-labeling showed all three these neuropathological structures also contained ubiquitin, synaptophysin, neurofilament (but not tau) immunoreactivity. contrast, neurofibrillary tangles, neuropil threads, Pick ballooned neurons, glial tangles (most which were tau positive) negative. These results support view specifically diseases related such suggests role for synaptic protein pathogenesis neurodegeneration.