The many faces of α-synuclein: from structure and toxicity to therapeutic target
By H. Lashuel, C. Overk, Abid Oueslati, E. Masliah. Nature Reviews Neuroscience, 2012
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Disorders characterized by α-synuclein (α-syn) accumulation, Lewy body formation and parkinsonism (and in some cases dementia) are collectively known as Lewy body diseases. The molecular mechanism (or mechanisms) through which α-syn abnormally accumulates and contributes to neurodegeneration in these disorders remains unknown. Here, we provide an overview of current knowledge and prevailing hypotheses regarding the conformational, oligomerization and aggregation states of α-syn and their role in regulating α-syn function in health and disease. Understanding the nature of the various α-syn structures, how they are formed and their relative contributions to α-syn-mediated toxicity may inform future studies aiming to develop therapeutic prevention and intervention.
Subfields: Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/7d27efa0a4a2b306eab272a85b279cf89885c922
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Citations in the corpus
- Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases (2015, background): “Microglial Phenotypes in PD PD is clinically manifested by progressive loss of dopaminergic (DA) neurons in the substantia nigra (SN) of the midbrain and pathologically characterized by the accumulation of protein aggregates called Lewy bodies (LBs) i n the remaining D A neurons [ 65, 66].”