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The human body has biological redox systems capable of preventing or mitigating the damage caused by increased oxidative stress throughout life. One of them are the paraoxonase (PON) enzymes. The PONs genetic cluster is made up of three members (PON1, PON2, PON3) that share a structural homology, located adjacent to chromosome seven. The most studied enzyme is PON1, which is associated with high density lipoprotein (HDL), having paraoxonase, arylesterase and lactonase activities. Due to these characteristics, the enzyme PON1 has been associated with the development of neurodegenerative diseases. Here we update the knowledge about the association of PON enzymes and their polymorphisms and the development of multiple sclerosis (MS), amyotrophic lateral sclerosis (ALS), Alzheimer's disease (AD) and Parkinson's disease (PD).
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7824310 | PMC |
http://dx.doi.org/10.3390/antiox10010011 | DOI Listing |
J Ethnopharmacol
March 2025
West China School of Basic Medical Sciences and Forensic Medicine, Sichuan University, Chengdu, 610041, China. Electronic address:
Mol Cell Probes
March 2025
Human and Neurobiology, Department of Chemistry and Biology, University of Siegen, Siegen, Germany. Electronic address:
Huntington's disease (HD) arises from the abnormal expansion of a CAG repeat in the HTT gene. The mutant CAG repeat triggers aberrant RNA-protein interactions and translates into toxic aggregate-prone polyglutamine protein. These aberrant RNA-protein ineractions also seed the formation of cytoplasmic liquid-like granules, such as stress granules.
View Article and Find Full Text PDFEur J Pharmacol
March 2025
Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, AlBeheira, Egypt. Electronic address:
Humanin (HN) is an endogenous micropeptide also known as a mitochondria-derived peptide. It has a neuroprotective effect against Alzheimer's disease (AD) and other neurodegenerative diseases by improving hippocampal acetylcholine and attenuating the development of oxidative stress and associated neurotoxicity. HN protects the neuron from the toxic effects of amyloid beta (Aβ).
View Article and Find Full Text PDFBrain Res
March 2025
Chitkara College of Pharmacy, Chitkara University, Punjab, India. Electronic address:
Synucleinopathies and amyloidogenic disorders are the two most prevalent neurodegenerative conditions, characterized by progressive loss of neurons and aggregation of proteins in the central nervous system. Emerging evidence suggests that despite their distinct pathological hallmarks: α-synuclein in Parkinson's disease (PD) and amyloid-β in Alzheimer's disease (AD), both disorders share common molecular pathways, including oxidative stress, neuroinflammation, misfolding/aggregation of proteins and mitochondrial dysfunction. This review explores the molecular intersections between synucleinopathies and amyloidogenesis.
View Article and Find Full Text PDFEur J Med Chem
March 2025
State Key Laboratory of Biotherapy and Cancer Center, Department of Neurology, West China Hospital, Sichuan University, Chengdu 610041, China. Electronic address:
Cell division cycle 7 (CDC7) plays an indispensable regulatory role in various cellular processes, encompassing the initiation of DNA replication and the maintenance of replication checkpoints. However, dysregulation of CDC7 protein levels is closely associated with the development and progression of several human diseases, particularly cancers and neurodegenerative diseases. Therefore, targeting the CDC7 kinase is deemed a potential avenue for disease management.
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