Prolongation of Chemically-Induced Methemoglobinemia in Mice Lacking α-synuclein: A Novel Pharmacologic and Toxicologic Phenotype.

ABSTRACT: The protein α -synuclein is considered central to the pathogenesis of Parkinson disease (PD) on genetic and histopathological grounds. It is widely expressed in fetal life and continues to be highly expressed in adult neural tissues, red blood cells and platelets, while the remainder of adult tissues are reported to have little or no expression. Despite cellular and molecular evidence for a role in neuronal function including synaptic vesicle trafficking, neurotransmitter release, mitochondrial function, lipid metabolism, neurogenesis, neuroprotection, and neuromelanin biosynthesis, mice ablated for the gene encoding α -synuclein (Snca) have little or no neurological phenotype. Thus, nearly 20 years of intensive study have yet to reveal conclusively what

SUBMITTER: Kuo YM 

PROVIDER: S-EPMC4386288 | biostudies-literature | 2015

REPOSITORIES: biostudies-literature