α-Synuclein Aggregation in Treatment of Parkinson's Disease

Parkinson’s disease, the second most common neurodegenerative disorder worldwide, is characterized by the accumulation of protein deposits in the dopaminergic neurons. These deposits are primarily composed of aggregated forms of α-Synuclein (α-Syn). PD is a complex pathology initially associated with motor deficiencies, as a result of an acute neuronal loss in substantia nigra pars compacta (SNc), with a significant dopaminergic (DA) impairment.

Current Progress in the Development of Probes for Targeting α-Synuclein Aggregates

Frontiers Modeling Parkinson's Disease With the Alpha-Synuclein Protein

Conformation-specific Antibodies Targeting Aggregated Forms of α-synuclein Block the Propagation of Synucleinopathy

Therapeutics in the Pipeline Targeting α-Synuclein for Parkinson's Disease

Initiation and progression of α-synuclein pathology in Parkinson's disease

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Regulation of α-synuclein homeostasis and inflammasome activation by microglial autophagy

Aggregated α-Synuclein Mediates Dopaminergic Neurotoxicity In Vivo

Suppression of abnormal α-synuclein expression by activation of BDNF transcription ameliorates Parkinson's disease-like pathology: Molecular Therapy - Nucleic Acids

p21-activated kinase 4 controls the aggregation of α-synuclein by reducing the monomeric and aggregated forms of α-synuclein: involvement of the E3 ubiquitin ligase NEDD4-1

Digesting recent findings: gut alpha-synuclein, microbiome changes in Parkinson's disease: Trends in Endocrinology & Metabolism

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Combating Parkinson's disease

α-Synuclein Aggregation in Treatment of Parkinson's Disease