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Existence of genetic variants of thiamine-dependent proteins, insufficient molecular identification of these proteins, as well as the age- and sex-dependent differences in thiamine metabolism (30), may contribute to the observed variety of clinical manifestations of thiamine deficiency (31, 32)

demonstrated that EGCG significantly increased the number of TH-immunoreactive neurons in the midbrain of PD model rats by reducing the production of TNF- and NO (170)

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Manuscript under review