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Alpha-synuclein-induced upregulation of SKI family transcriptional corepressor 1: a new player in aging & Parkinson's disease?
Neural Regen Res
December 2024
Department of Anatomy and Neuroscience, School of Medicine, University College Cork, Cork, Ireland (Barrett L, Bevans R, Collins LM, O'Keeffe GW).
2-Butoxytetrahydrofuran, Isolated from , Attenuates Aggregative and Oxidative Properties of α-Synuclein and Alleviates Its Toxicity in a Transgenic Model of Parkinson's Disease.
ACS Chem Neurosci
June 2024
Department of Anatomy, Faculty of Science, Mahidol University, Ratchathewi, Bangkok 10400, Thailand.
Aggregative α-synuclein and incurring oxidative stress are pivotal cascading events, leading to dopaminergic (DAergic) neuronal loss and contributing to clinical manifestations of Parkinson's disease (PD). Our previous study demonstrated that 2-butoxytetrahydrofuran (2-BTHF), isolated from (), could inhibit amyloid-β aggregation and its ensuing toxicity, which leads to Alzheimer's disease. In the present study, we found that 2-BTHF also attenuated the aggregative and oxidative activities of α-synuclein and lessened its toxicity in a transgenic () PD model.
View Article and Find Full Text PDFElevated α-synuclein levels inhibit mitophagic flux.
NPJ Parkinsons Dis
April 2024
Department of Neurosciences, Laboratory for Parkinson Research, KU Leuven, Leuven, Belgium.
The pathogenic effect of SNCA gene multiplications indicates that elevation of wild-type α-synuclein levels is sufficient to cause Parkinson's disease (PD). Mitochondria have been proposed to be a major target of α-synuclein-induced damage. PINK1/parkin/DJ-1-mediated mitophagy is a defense strategy that allows cells to selectively eliminate severely damaged mitochondria.
View Article and Find Full Text PDFα-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce Ca3.2 calcium signaling in astrocytes.
Transl Neurodegener
February 2024
Department of Chemistry, School of Sciences, National and Kapodistrian University of Athens, Panepistimioupolis Zografou, 15772, Athens, Greece.
Background: It is now realized that Parkinson's disease (PD) pathology extends beyond the substantia nigra, affecting both central and peripheral nervous systems, and exhibits a variety of non-motor symptoms often preceding motor features. Neuroinflammation induced by activated microglia and astrocytes is thought to underlie these manifestations. α-Synuclein aggregation has been linked with sustained neuroinflammation in PD, aggravating neuronal degeneration; however, there is still a lack of critical information about the structural identity of the α-synuclein conformers that activate microglia and/or astrocytes and the molecular pathways involved.
View Article and Find Full Text PDFAdenosine A receptor antagonist KW6002 protects against A53T mutant alpha-synuclein-induced brain damage and neuronal apoptosis in Parkinson's disease mice by restoring autophagic flux.
Neurosci Lett
March 2024
Department of Ophthalmology, Wenzhou Medical University Ningbo Eye Hospital, Ningbo 315040, China.
Background: Protein misfolding and inclusion body aggregation caused by α-Syn mutations in the brain often cause neurodegeneration and cognitive impairment, among which the A53T point mutation is more common. Inhibition of adenosine A2A receptor (AR) can alleviate the pathological symptoms of brain dysfunction caused by A53T-α-Syn protofibrils, but the mechanism of action is still unclear.
Aim: This studies aimed to investigate the potential therapeutic role of the AR inhibitor KW6002 in a mouse model of brain synucleinopathy.
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