Alpha-synuclein spreading in M83 mice brain revealed by detection of pathological α-synuclein by enhanced ELISA.

ABSTRACT:

Background

The accumulation of misfolded proteins appears as a fundamental pathogenic process in human neurodegenerative diseases. In the case of synucleinopathies such as Parkinson's disease (PD) or dementia with Lewy bodies (DLB), the intraneuronal deposition of aggregated alpha-synuclein (αS) is a major characteristic of the disease, but the molecular basis distinguishing the disease-associated protein (αSD) from its normal counterpart remains poorly understood. However, recent research suggests that a prion-like mechanism could be involved in the inter-cellular and inter-molecular propagation of aggregation of the protein within the nervous system.

Results

Our data confirm our previous observations of disease acceleration in a transgenic mouse line (M83) overexpressing a

SUBMITTER: Betemps D 

PROVIDER: S-EPMC4007641 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature