Although the function of<unk>  is not well understood, studies suggest that it plays a role in restricting the mobility of<unk> aptic vesicles, consequently attenuating<unk> aptic vesicle recycling and neurotransmitter release. An alternate view is that<unk>  binds to VAMP2 (a<unk> aptobrevin) and stabilizes SNARE complexes; though recent studies indicate that<unk> –VAMP2 binding is critical for<unk> -mediated attenuation of<unk> aptic vesicle recycling, connecting the two seemingly divergent views. It may also help regulate the release of dopamine, a type of neurotransmitter that is critical for controlling the start and stop of voluntary and involuntary movements.<unk>  modulates DNA repair processes, including repair of double-strand breaks (DSBs). DNA damage response markers co-localize with<unk>  to form discrete foci in human cells and mouse brain. Depletion of<unk>  in human cells causes increased introduction of DNA DSBs after exposure to bleomycin and reduced ability to repair these DSBs. In addition,<unk>  knockout mice display a higher level of DSBs, and this problem can be alleviated by transgenic reintroduction of human<unk> .<unk>  promotes the DSB repair pathway referred to as non-homologous end joining. The DNA repair function of<unk>  appears to be compromised in Lewy body inclusion bearing neurons, and this may trigger cell death. Proneurogenic function of<unk>  In some neurodegenerative diseases,<unk>  produces insoluble inclusion bodies. These diseases, known as<unk> ucleinopathies, are connected with either higher levels of normal<unk>  or its mutant variants. The normal physiological role of Snca, however, has not yet been thoroughly explained. In fact, physiological Snca has been demonstrated to have a neuroprotective impact by inhibiting apoptosis induced by several types of apoptotic stimuli, or by regulating the expression of proteins involved in apoptotic pathways. Recently it has been demonstrated that up-regulation of<unk>  in the dentate gyrus (a neurogenic niche where new neurons are generated throughout life) activates stem cells, in a model of premature neural aging. This model shows reduced expression of<unk>  and reduced proliferation of stem cells, as is physiologically observed during aging. Exogenous<unk>  in the dentate gyrus is able to rescue this defect. Moreover,<unk>  also boosts the proliferation of dentate gyrus progenitor neural cells in wild-type young mice. Thus,<unk>  represents an effector for neural stem and progenitor cell activation. Similarly,<unk>  has been found to be required to maintain stem cells of the SVZ (subventricular zone, i.e., another neurogenic niche) in a cycling state.
Alpha-synuclein
Kamino bodies
Lewy body
Neurofibrillary tangle
Amyloid beta
Neurofilament light polypeptide
Hirano body
Wild-type transthyretin amyloid