The ATP-sensitive potassium（KATP）channels which extensively distribute in diverse tissues（e.g.vascular smooth muscle,cardiac cells,and pancreas）are well-established for characteristics like vasodilatation,myocardial protection against ischemia,and insulin secretion.The aim of this review is to get insight into the novel roles of KATPchannels in Parkinson＇s disease（PD）,with consideration of the specificities KATPchannels in the central nervous system（CNS）, such as the control of neuronal excitability,action potential,mitochondrial function and neurotransmitter release.
SK channels are small conductance calcium-activated potassium channels that are widely expressed in different neurons with distinct subtypes.They play an important role in modulating synaptic plasticity,dopaminergic neurotransmission, and learning and memory.The present review was mainly focused on the recent findings on the contradictory roles of SK channels in modulating dopaminergic neurons in substantia nigra and in the pathogenesis of Parkinson＇s disease （PD） . Besides,whether modulation of SK channels could be a potential target for PD treatment was also discussed.
The growth factor receptor-bound protein 2 （Grb2） -associated binder （Gab） proteins are intracellular scaffolding/ docking molecules,and participate in multiple signaling pathways,usually acting as the downstream effector of protein-tyrosine kinases （PTKs） -triggered signal transduction pathway.When phosphorylated by PTKs,Gab proteins can recruit several signaling molecules （p85,SHP2,and Crk） ,and subsequently activate multiple transmitting signals that are critical for cell growth,survival,differentiation and apoptosis.Recently,it has been reported that Gab2 polymorphism is associated with the increase in the risk of Alzheimer’s disease （AD） and is involved in the pathogenesis of AD.This review mainly focuses on the structure and function of Gab2 protein and its role in the pathogenesis of AD.
Inflammation has been shown to play an important role in the progression of Alzheimer＇s disease （AD）. Recent epidemical study indicates that the incidence of AD in some populations is substantially influenced by the gene polymorphisms of the inflammation mediators. Meanwhile, an ensured risk factor, the ApoE ε4 allele is also reported to directly promote inflammation. Accordingly, it appears that an individual genetic background has partly determined his predisposition for AD by the extent of the inflammation response to the chronic stimulus by β-amyloid peptide （Aβ） deposits and other antigen stressor in the elderly. Hence we present a hypothesis that the inflammation genotypes may contribute to AD susceptibility. This may provide a new orientation both for future identification of individuals at risk and for personalized medication.
