Parkinson's Disease (PD) is the neurodegenerative disease with high frequency next to Alzheimer Disease. It is characterized by loss of dopaminergic neurons in a substantia nigra and the appearance of Lewy bodies, therefore PD is a kind of progressive malignant disease to cause muscle rigidity and tremor. In the brain, spinal cord and olfactory bulb, the Lewy body is composed of the protein α -Synuclein, phosphorylated α -Synuclein and also including other proteins. Abnormal aggregation of α -Synuclein and phosphorylated α -Synuclein is accepted at high frequency in neuronal cells of PD patients. It is suspected that abnormal accumulations of α -Synuclein trigger neurodegeneration. To clarify where the Lewy bodies and phosphorylated α -Synuclein appear, it is necessary to establish the non-human primate model.
In our laboratory, a novel non-human primate model of PD using mutated α -Synuclein (A30P) was established to explore the effect of mutated α -Synuclein. As for the common marmoset (Callithrix jacchus ), a small New World primate, its structure of the brain evolves in comparison with rodents. Therefore, we expect that it is possible to link between an exercise dysfunction and a lesion part because the structure of the basal nuclei which are a main lesion part of PD is clear in marmoset. The transgene of mutated α -Synuclein (A30P) expression was evident in the brain of transgenic marmoset, moreover we found the abnormal protein aggregations in the liver. Thus we searched for a Lewy body in the all tissues and organs of transgenic marmoset including skin. In this presentation, we will show the recent results of searching Lewy body and also the exercise functional analysis.