Automated Capillary Electrophoresis Immunoblot for the Detection of Alpha-Synuclein in Mouse Tissue.

Background: Alpha-synuclein (aSyn) is a key player in neurodegenerative diseases such as Parkinson's disease (PD), dementia with Lewy bodies, or multiple system atrophy. aSyn is expressed throughout the brain, and can also be detected in various peripheral tissues. In fact, initial symptoms of PD are non-motoric and include autonomic dysfunction, suggesting that the periphery might play an important role in early development of the disease.

Protein trapping leads to altered synaptic proteostasis in synucleinopathies.

Parkinson's disease (PD) is associated with the accumulation of alpha-synuclein (aSyn) in intracellular inclusions known as Lewy bodies and Lewy neurites. Under physiological conditions, aSyn is found at the presynaptic terminal and exists in a dynamic equilibrium between soluble, membrane-associated and aggregated forms. Emerging evidence suggests that, under pathological conditions, aSyn begins to accumulate and acquire a toxic function at the synapse, impairing their normal function and connectivity.

Synucleinopathies: Where we are and where we need to go.

Synucleinopathies are a group of disorders characterized by the accumulation of inclusions rich in the a-synuclein (aSyn) protein. This group of disorders includes Parkinson's disease, dementia with Lewy bodies (DLB), multiple systems atrophy, and pure autonomic failure (PAF). In addition, genetic alterations (point mutations and multiplications) in the gene encoding for aSyn (SNCA) are associated with familial forms of Parkinson's disease, the most common synucleinopathy.