Parkinson's disease (PD) is characterized by gradual neurodegeneration and forfeiture of dopamine neurons in substantia nigra pars compacta which ultimately leads to depletion of dopamine levels. PD patients not only display motor features such as rigidity, tremor, and bradykinesia but also non-motor features such as depression, anxiety, etc. Various treatments are available for PD patients such as dopamine replacement are well established but it is only partially or transiently effective. As these therapies not able to restore dopaminergic neurons and delay the development of Parkinson's disease, therefore, the need for an effective therapeutic approach is crucial. The present review discusses a comprehensive overview of current novel targets for PD which includes molecular chaperone, neuroinflammation, mitochondrial dysfunction, neuromelanin, Ubiquitin-proteasome system, protein Abelson, Synaptic vesicle glycoprotein 2C, and Cocaine-amphetamine-regulated transcript, etc. These approaches will help to identify new targets for the treatment of disease and may provide a ray of hope for PD patient treatment. Graphical abstract.
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http://dx.doi.org/10.1007/s11011-020-00636-w | DOI Listing |
PLoS One
January 2025
Institute of Psychiatry, Psychology & Neuroscience at King's College London, London, United Kingdom.
Fluctuation-related pain (FRP) affects more than one third of people with Parkinson's disease (PwP, PD) and has a harmful effect on health-related quality of life (HRQoL), but often remains under-reported by patients and neglected by clinicians. The National Institute for Health and Care Excellence (NICE) recommends The Parkinson KinetiGraphTM (the PKGTM) for remote monitoring of motor symptoms. We investigated potential links between the PKGTM-obtained parameters and clinical rating scores for FRP in PwP in an exploratory, cross-sectional analysis of two prospective studies: "The Non-motor International Longitudinal, Real-Life Study in PD-NILS" and "An observational-based registry of baseline PKG™ in PD-PKGReg".
View Article and Find Full Text PDFOper Neurosurg (Hagerstown)
September 2024
Department of Neurology, Washington University in St Louis, St Louis, Missouri, USA.
Background And Objectives: Surgical planning is critical to achieve optimal outcome in deep brain stimulation (DBS). The relationship between clinical outcomes and DBS electrode position relative to subthalamic nucleus (STN) is well investigated, but the role of surgical trajectory remains unclear. We sought to determine whether preoperatively planned DBS lead trajectory relates to adequate motor outcome in STN-DBS for Parkinson's disease (PD).
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Department of Neurology, Oregon Health and Science University, 3181 SW Sam Jackson Park Road, Portland, OR, 97239, USA.
Neuroinflammation and mitochondrial dysfunction are early events in Alzheimer's disease (AD) and contribute to neurodegeneration and cognitive impairment. Evidence suggests that the inflammatory axis mediated by macrophage migration inhibitory factor (MIF) binding to its receptor, CD74, plays an important role in many central nervous system (CNS) disorders such as AD. Our group has developed DRhQ, a novel CD74 binding construct which competitively inhibits MIF binding, blocks macrophage activation and migration into the CNS, enhances anti-inflammatory microglia cell numbers and reduces pro-inflammatory gene expression.
View Article and Find Full Text PDFJ Neuroimmune Pharmacol
January 2025
Department of Cardiothoracic Surgery, Children's Hospital of Nanjing Medical University, Nanjing, 210008, China.
Parkinson's disease (PD) is a complex progressive neurodegenerative disorder and the pathogenesis and treatment methods are unknown. This aim is to investigate the effects of long non coding RNA NEAT1 (LncRNA NEAT1) on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinson's disease (PD). Immunoprecipitation and western blot were used to search for the effects of LncRNA NEAT1 on PD.
View Article and Find Full Text PDFASN Neuro
January 2025
School of Life Science and Technology, ShanghaiTech University, Shanghai, China.
We previously identified a role for dAuxilin (dAux), the fly homolog of Cyclin G-associated kinase, in glial autophagy contributing to Parkinson's disease (PD). To further dissect the mechanism, we present evidence here that lack of glial dAux enhanced the phosphorylation of the autophagy-related protein Atg9 at two newly identified threonine residues, T62 and T69. The enhanced Atg9 phosphorylation in the absence of dAux promotes autophagosome formation and Atg9 trafficking to the autophagosomes in glia.
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