Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
6018163 | Experimental Neurology | 2013 | 5 Pages |
Abstract
The presynaptic protein α-synuclein is central to the pathogenesis of α-synucleinopathies. We show that the presence of endogenous mouse α-synuclein leads to higher number of dopaminergic neurons in the substantia nigra of wild-type C57Bl/6J mice compared with C57Bl/6S mice with a spontaneous deletion of the α-synuclein gene or C57Bl/6J mice with a targeted deletion of the α-synuclein gene. This effect of α-synuclein on dopaminergic neuron occurs during development between E10.5 and E13.5 and persists in adult life supporting the involvement of α-synuclein in the development of a subset of dopaminergic neurons.
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Authors
Pablo Garcia-Reitboeck, Oleg Anichtchik, Jeffrey W. Dalley, Natalia Ninkina, George K. Tofaris, Vladimir L. Buchman, Maria Grazia Spillantini,