Key Points Question Does the pathological α-synuclein (αSyn P ) detected by immunohistochemistry in the skin of individuals with Parkinson disease (PD) have aggregation seeding activity, and is skin αSyn P seeding activity a potential biomarker for diagnosis of PD and other synucleinopathies?
protein aggregationinflammationA growing body of evidence indicates that an inflammatory process in the substantia nigra, characterized by activation of resident microglia, likely either initiates or aggravates nigral neurodegeneration in Parkinson's disease (PD). To study the mechanisms by which nigral ...
Using these sensor chips, we evaluated diet-derived catechols dihydrocaffeic acid and caffeic acid as potential inhibitors of α-synuclein aggregation. Our results suggest that these molecules inhibit dopamine oxidation. We also found that these dietary catechols inhibit α-synuclein aggregation in STC...
progression of PD has provided insights into PD pathology. This review will provide a brief overview of increasing researches that shed light on the relationship of α-syn aggregation with mitochondrial and lysosomal dysfunctions, and highlight recent understanding of α-syn transmission in PD ...
Parallel findings were observed in mouse brain: PFF-induced α-synuclein aggregation in the substantia nigra was associated with redox stress, c-Abl activation, and dopaminergic neuronal loss, along with microglial activation and motor impairment, all of which were attenuated with oral N-acetyl ...
The aggregation of αSYN seems to be the central driver of the pathogenesis of synucleinopathies; however, the relationship between αSYN misfolding and cellular dysfunction or cell death is far from fully understood. The removal of αSYN aggregates holds considerable promise as a therapeutic ...
This suggests several options. Synuclein is the obvious primary target, and options include including passive immunotherapy, active immunotherapy, aggregation inhibitors, antisense oligonucleotides, etc. Lysosomal dysfunction also seems to be a critical in iRBD pathophysiology, and agents targeting glucocerebro...
Targeting of extracellular α-synuclein—for example, promoting its clearance—might be a promising therapeutic strategy for modifying the progression of Lewy body diseases Abstract Misfolding and intracellular aggregation of α-synuclein are thought to be crucial factors in the pathogenesis of Lewy body...
However, it has not yet been investigated whether other aggregation-prone proteins are able to induce SOD1 oligomerization in vivo. This could give rise to a different therapeutic strategy: not to target SOD1 aggregates directly but to reduce the trigger for aggregate formation. Because tau and ...
While the influence of NPY on aSyn aggregation is yet to be clarified, the peptide possesses all the essential physicochemical attributes to effectively bind to aSyn’s toxic forms. In addition, NPY is predicted to be non-toxic and cell-penetrating. This information supports a re-examination of...