α-synuclein toxicity in neurodegeneration: mechanism and therapeutic strategies
By Y. Wong, D. Krainc. Nature Medicine, 2017
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Alterations in α-synuclein dosage lead to familial Parkinson's disease (PD), and its accumulation results in synucleinopathies that include PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Furthermore, α-synuclein contributes to the fibrilization of amyloid-b and tau, two key proteins in Alzheimer's disease, which suggests a central role for α-synuclein toxicity in neurodegeneration. Recent studies of factors contributing to α-synuclein toxicity and its disruption of downstream cellular pathways have expanded our understanding of disease pathogenesis in synucleinopathies. In this Review, we discuss these emerging themes, including the contributions of aging, selective vulnerability and non-cell-autonomous factors such as α-synuclein cell-to-cell propagation and neuroinflammation. Finally, we summarize recent efforts toward the development of targeted therapies for PD and related synucleinopathies.
Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/29b9da3a80ab8d05eeac66986a4a717ad017d6c9
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In Cellular and Molecular Neuroscience
In Neurology
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Citations in the corpus
- Hallmarks of Brain Aging: Adaptive and Pathological Modification by Metabolic States (2018, background): “…that result in aberrant accumulation of a-synuclein aggregates, which can overload the autophagy pathway and cause mitochondrial dysfunction (Wong and Krainc, 2017), and autosomal recessive mutations in Parkin and PINK1, which impair the ability of neurons to recognize and remove (via…”