Date: April 25, 2023
Time: 10:00 a.m. (PDT), 1:00 p.m. (EDT), 7:00 p.m. (CEST)
The presynaptic protein alpha-synuclein (α-syn) is associated with Parkinson’s disease and Lewy body dementia. Aggregated and post-translationally modified α-syn forms accumulate in the central and peripheral nervous system at various disease stages. Neuronal dysfunction can be the result of a decrease in native α-syn, but also due to the accumulation of aberrant α-syn forms. These α-syn forms are still largely uncharacterized and can cause cell death. In this seminar, we will discuss i) an overview of the progression of Parkinson’s disease pathology, i.e., α-syn aggregate accumulation and spreading in the nervous system; ii) an overview of aberrant α-syn forms present in human tissue; iii) a hypothesis on how accumulation of α-syn aggregates in neurons causes functional defects that contribute to patients’ symptomatology – defects that may progress for years before the neurons die. The presence of functional defects in viable neurons allows for therapeutic strategies to counteract the dysfunctions, and thereby ease the patient’s symptoms and slow disease progression.
- Different parts of the nervous system, central and peripheral, are affected during progressive stages of Parkinson’s disease.
- During disease progression, α-syn changes both its structure, based on its aggregation into various forms and posttranslational modifications, and its subcellular localization.
- The progressive build-up of aberrant α-syn species holds potential for inducing specific neuronal dysfunctions that may be targetable by new disease management strategies.
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