パーキンソン病細胞モデルにおけるニコチン受容体を介したオートファジー活性化の分子機構に関する研究

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  • Study of the molecular mechanism of autophagy activation<i> via </i>nicotine receptors in a cellular model for Parkinson‘s disease

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<p>[Background] Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) have increasingly been realized to have common cellular and molecular mechanisms including protein aggregation and inclusion body formation. In the present study, to examine whether the activation of a7 nicotinic receptor has neuroprotective effect against PD-associated mutant a-synuclein-induced aggregation and neurotoxicity in a cellular model, we used nicotine and PNU 282987, an a7 nicotinic receptor agonist.</p><p>[Methods] To investigate the effect of nicotine and PNU 282987 against mutant a-synuclein aggregates, we evaluated the protein level of a-synuclein in a cellular model of PD.</p><p>[Results] We succeeded in generating a new α-Syn stably expressing cell line using a piggyBac transposon system. Using this system, we investigated the neuroprotective effect of the nicotine and PNU 282987 on a-synuclein toxicity. We found that PNU 282987 provided significant protection against a-synuclein-related neurotoxicity. These results suggest that nicotine and PNU 282987 reduced intracellular aggregate via the activation of autophagy.</p><p>[Conclusions] Nicotine as well as PNU 282987 against a-synuclein-induced aggregation via the activation of autophagy are an efficient source of new treatment and prevention for synucleinopathies.</p>

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