Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1002/mds.26255 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Mitochondrial dysfunction in Parkinson's disease.
J Neural Transm (Vienna)
December 2024
Department of Neurology, Faculty of Medicine, Juntendo University, 2-1-1 Hongo, Bunkyo, Tokyo, 113-8421, Japan.
Article Synopsis
- The exact cause of nigral cell death in Parkinson's disease (PD) is still unclear, but research has made significant progress using models like MPTP-induced experimental parkinsonism, highlighting mitochondrial failure as a key factor in cell death.
- Many studies have linked mitochondrial dysfunction to PD, observing deficiencies in mitochondrial complexes (specifically Complex I and III) in various tissues of PD patients, though there’s some debate on its impact in peripheral organs.
- Mutations in mitochondrial DNA and involvement of specific genes related to mitochondrial quality control (like parkin and PINK1) further suggest that mitochondrial issues play a crucial role in the pathophysiology of PD.
AdipoRon improves mitochondrial homeostasis and protects dopaminergic neurons through activation of the AMPK signaling pathway in the 6-OHDA-lesioned rats.
Eur J Pharmacol
December 2024
Department of Biomedical Education, California Health Sciences University, College of Osteopathic Medicine, Clovis, CA, USA. Electronic address:
The progressive decline of dopaminergic neurons in Parkinson's disease (PD) has been linked to an imbalance in energy and the failure of mitochondrial function. AMP-activated protein kinase (AMPK), the major intracellular energy sensor, regulates energy balance, and damage to nigral dopaminergic neurons induced by 6-hydroxydopamine (6-OHDA) is exacerbated in the absence of AMPK activity. This study aimed to examine the potential therapeutic advantages of AdipoRon, an AMPK activator, on motor function and mitochondrial homeostasis in a 6-OHDA-induced PD model.
View Article and Find Full Text PDFLRRK2 regulates production of reactive oxygen species in cell and animal models of Parkinson's disease.
Sci Transl Med
October 2024
Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Article Synopsis
- Scientists think that oxidative stress, which means damage from too many harmful substances in the body, is linked to Parkinson's disease (PD).
- A specific gene called LRRK2 has mutations that make it more active and can increase the risk of getting PD, and this is related to more oxidative stress.
- In studies with special lab techniques and cells from people with PD, it was found that blocking LRRK2 activity helps reduce harmful reactions, suggesting that controlling LRRK2 could help manage oxidative stress in PD.
The Tree Shrew Model of Parkinson Disease: A Cost-Effective Alternative to Nonhuman Primate Models.
Lab Invest
November 2024
National Research Facility for Phenotypic & Genetic Analysis of Model Animals (Primate Facility), Key Laboratory of Genetic Evolution & Animal Models, and National Resource Center for Nonhuman Primates, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China; Key Laboratory of Animal Models and Human Disease Mechanisms of Yunnan Province, and KIZ/CUHK Joint Laboratory of Bioresources and Molecular Research in Common Diseases, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, China. Electronic address:
The surge in demand for experimental monkeys has led to a rapid increase in their costs. Consequently, there is a growing need for a cost-effective model of Parkinson disease (PD) that exhibits all core clinical and pathologic phenotypes. Evolutionarily, tree shrews (Tupaia belangeri) are closer to primates in comparison with rodents and could be an ideal species for modeling PD.
View Article and Find Full Text PDFModulation of cannabinoid receptor 2 alters neuroinflammation and reduces formation of alpha-synuclein aggregates in a rat model of nigral synucleinopathy.
J Neuroinflammation
September 2024
Department of Neuroscience, University of Florida College of Medicine, Gainesville, FL, USA.
Research into the disequilibrium of microglial phenotypes has become an area of intense focus in neurodegenerative disease as a potential mechanism that contributes to chronic neuroinflammation and neuronal loss in Parkinson's disease (PD). There is growing evidence that neuroinflammation accompanies and may promote progression of alpha-synuclein (Asyn)-induced nigral dopaminergic (DA) degeneration. From a therapeutic perspective, development of immunomodulatory strategies that dampen overproduction of pro-inflammatory cytokines from chronically activated immune cells and induce a pro-phagocytic phenotype is expected to promote Asyn removal and protect vulnerable neurons.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!