Gender Differences in Neurodegeneration, Neuroinflammation and Na+-Ca2+ Exchangers in the Female A53T Transgenic Mouse Model of Parkinson's Disease.

摘要: Twelve-month-old male mice expressing the human A53T variant of α-synuclein (A53T) develop dopamine neuron degeneration, neuroinflammation, and motor deficits, along with dysfunctions mitochondrial Na+-Ca2+ exchanger (NCX) isoforms 1 (NCX1) 3 (NCX3) in nigrostriatal system. Since gender is thought to play a role etiology Parkinson's disease (PD), we characterized neurochemical behavioral alterations 12-month-old female transgenic mice. We investigated presence dopaminergic astrogliosis microgliosis using immunohistochemistry for tyrosine hydroxylase (TH), glial fibrillary acidic protein (GFAP) ionized calcium-binding adaptor molecule-1 (IBA-1) both substantia nigra pars compacta (SNc) striatum. In same regions, also evaluated co-localization NCX1 cells positive IBA-1 NCX3 TH-positive neurons fibers. Furthermore, mice, performed (beam walking pole tests) memory [novel object recognition (NOR) spontaneous alternation] tasks, together tests evaluate peripheral deficits (olfactory stool collection tests). Female displayed degeneration nigral neurons, but neither nor SNc Moreover, between striatum not SNc, whereas did co-localize either terminals or neuronal bodies showed increased crossing time beam test, no impairments tests, that motor, deficits. Immunohistochemical results obtained here differ from those previously observed males, suggest dissimilar influence on function strengthening validity these as model studying etiological factors PD.