Heterogeneity in α-synuclein fibril activity correlates to disease phenotypes in Lewy body dementia
Authors (first, second and last of 13)
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Emerging concepts in synucleinopathies
Alpha-synuclein (aSyn) is a central player in age-associated disorders known as synucleinopathies, where it accumulates in intracellular protein inclusions. Synucleinopathies include Parkinson’s disease (PD), Dementia with Lewy bodies (DLB), and multiple systems atrophy (MSA), all of which are highly debilitating age-associated disorders. Neuropathology studies show us that the old brain is multi-morbid, with the simultaneous accumulation of various types of protein pathologies that have been, traditionally, associated with individual diseases [1]. We assume that during the process of protein aggregation, different types of aggregated species (oligomers, protofibrils, fibrils, etc) are formed, and that at least some might be toxic to cells/tissues/organs, thereby leading to neurodegeneration. However, we still cannot definitively establish this causal relationship between protein aggregation and disease.
Editors
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Tiago Fleming Outeiro
Professor Outeiro holds positions as Professor of Proteinopathies and Neuroscience at the Universities of Goettingen and Newcastle respectively. His research interests are focused on the understanding of the molecular mechanisms which lead to neurodegeneration in diseases such as Parkinson’s, Huntington’s, or Alzheimer’s disease. These diseases are intimately associated with protein misfolding and aggregation in specific regions of the brain.
Articles (6 in this collection)
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Lipids, lysosomes and mitochondria: insights into Lewy body formation from rare monogenic disorders
Authors (first, second and last of 6)
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