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• W4307486516 abstract "Synucleinopathies such as Parkinson’s disease, dementia with Lewy bodies and multiple system atrophy are characteristic for α -synuclein aggregates in neurons or glia, and are always manifested olfaction deficits at their primary onsets. It remains elusive why aggregation of α -synuclein predominantly affect the olfactory system. Employing the knockout mice, we investigate the physiological function of α-synuclein in olfactory system. We found that deletion of α-synuclein primarily interferes the projection of olfactory sensory neurons. iTRAQ based LC-MS identified that 188 proteins are differentially expressed, including 9 that were associated with axon guidance. Among them, NCK2 is most significantly down-regulated, which was indicated to be involved a PPI network of 21 proteins, including 11 players of the Ephrin receptor signaling pathway. Either α-synuclein deletion or NCK2 deficiency can inactivate Eph A4 receptor. Re-expressing α-synuclein in the α-synuclein knockout neurons reverse the NCK2, as well as the phosphorylated Eph A4 (the activated Eph A4). Thus, α-synuclein regulates axon guidance through NCK2-Eph A4 signaling pathway. Malfunction of α-synuclein, whether because of deletion or aggregation, may cause aberrant olfactory neurons projection and subsequent olfaction deficits. This extended our knowledge of effects of α-synuclein in olfactory system, which may explain why olfaction is usually impaired in some synucleinopathy related disorders such as Parkinson’s disease." @default.
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• W4307486516 date "2022-10-25" @default.
• W4307486516 modified "2023-10-18" @default.
• W4307486516 title "SNCA Deletion Induced Aberrant Projection of Olfactory Sensory Neurons via NCK2-EphA4 Pathway" @default.
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• W4307486516 doi "https://doi.org/10.1101/2022.10.25.513708" @default.
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