Parkinson's disease (PD) may optimally be treated with a disease-modifying therapy to slow progression. We compare data underlying surgical approaches proposed to impart disease modification in PD: (1) cell transplantation therapy with stem cell-derived dopaminergic neurons to replace damaged cells; (2) clinical trials of growth factors to promote survival of existing dopaminergic neurons; (3) subthalamic nucleus deep brain stimulation early in the course of PD; and (4) abdominal vagotomy to lower risk of potential disease spread from gut to brain. Though targeted to engage potential mechanisms of PD these surgical approaches remain experimental, indicating the difficulty in translating therapeutic concepts into clinical practice. The choice of outcome measures to assess disease modification separate from the symptomatic benefit will be critical to evaluate the effect of the disease-modifying intervention on long-term disease burden, including imaging studies and clinical rating scales, i.e., Unified Parkinson Disease Rating Scale. Therapeutic interventions will require long follow-up times (i.e., 5-10 years) to analyze disease modification compared to symptomatic treatments. The promise of invasive, surgical treatments to achieve disease modification through mechanistic approaches has been constrained by the reality of translating these concepts into effective clinical trials.
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http://dx.doi.org/10.1038/s41531-022-00296-w | DOI Listing |
BMC Nurs
January 2025
The First Affiliated Hospital of China Medical University, No.155, Nanjing North Street, Heping District, Shenyang, Liaoning Province, China.
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View Article and Find Full Text PDFBMC Public Health
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Department of Occupational Health Practice and Management, Institute of Industrial Ecological Sciences, University of Occupational and Environmental Health, Fukuoka, Japan.
Background: During the COVID-19 pandemic, information and circumstances changed from moment to moment, including the accumulation of scientific knowledge, the emergence of variants, social tolerance, and government policy. Therefore, it was important to adapt workplace countermeasures punctually and flexibly based on scientific evidence and according to circumstances. However, there has been no assessment of changes in workplace countermeasures.
View Article and Find Full Text PDFMol Med
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Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, China.
Background: Mitochondrial dysfunction and neuronal damage are major sign of cytopathology in Huntington's disease (HD), a neurodegenerative disease. Ubiquitin specific peptidase 11 (USP11) is a deubiquitinating enzyme involved in various physiological processes through regulating protein degradation. However, its specific role in HD is unclear.
View Article and Find Full Text PDFNat Commun
January 2025
Proteomics and Bioanalytics, School of Life Sciences, Technical University of Munich, Freising, Germany.
Post-translational modifications (PTMs) play pivotal roles in regulating cellular signaling, fine-tuning protein function, and orchestrating complex biological processes. Despite their importance, the lack of comprehensive tools for studying PTMs from a pathway-centric perspective has limited our ability to understand how PTMs modulate cellular pathways on a molecular level. Here, we present PTMNavigator, a tool integrated into the ProteomicsDB platform that offers an interactive interface for researchers to overlay experimental PTM data with pathway diagrams.
View Article and Find Full Text PDFJ Neurosci
January 2025
Neuroapoptosis Laboratory, Department of Neurological Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213;
Huntington's disease (HD), a neurodegenerative disease, affects approximately 30,000 people in the United States, with 200,000 more at risk. Mitochondrial dysfunction caused by mutant huntingtin (mHTT) drives early HD pathophysiology. mHTT binds the translocase of mitochondrial inner membrane (TIM23) complex, inhibiting mitochondrial protein import and altering the mitochondrial proteome.
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