On the Role of α-synuclein in Parkinson's Disease

Parkinson's disease, like dementia with Lewy bodies, is a synucleinopathy, a condition characterized by the buildup of aggregates of misfolded, toxic α-synuclein that cause cell death in the brain. The mix of age-related cellular damage, evolved reactions to that damage, and individual genetic variance that leads to the creation of these aggregates is highly complex and poorly understood. As for other diseases involving forms of protein aggregate that harm tissues, such as the varied forms of amyloidosis, one possible shortcut to meaningful treatment is to clear the aggregates on a regular basis. The research community is making some inroads in this direction, such as the production of immunotherapies that can target misfolded proteins, but it has been slow going so far: Accumulation and misfolding of the α-synuclein protein are core mechanisms in the pathogenesis of Parkinson's disease. While the normal function of alpha-synuclein is mainly related to the control of vesicular neurotransmission, its pathogenic effects are linked to various cellular functions, which include mitochondrial activity, as well as proteasome and autophagic degradation of proteins. Remarkably, these functions are also affected when the renewal of macromolecules and organelles becomes impaired during the normal aging process. As aging is considered a major risk factor for Parkinson's disease, it is critical to explore its molecular and cellular implications in the context of the alpha-synuclein pat...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs