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Do Novel Nonexercise and Nondrug Treatments Improve Global Cognition in Parkinson's Disease Patients? A Systematic Review and Bayesian Analysis.
Eur J Neurosci
February 2025
Department of Neurology, Guangdong Neuroscience Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.
This Bayesian network meta-analysis method was used to assess the effect of novel treatments on global cognition in patients with Parkinson's disease (PD). We searched randomized controlled trials from PubMed, Cochrane Library, Web of Science and Embase to investigate novel treatments for global PD cognition until April 10, 2024. Effect size measures were standardized mean differences with 95% confidence intervals.
View Article and Find Full Text PDFAdeno-associated viral vectors for modeling Parkinson's disease in non-human primates.
Neural Regen Res
January 2025
CNS Gene Therapy Department, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain.
The development of clinical candidates that modify the natural progression of sporadic Parkinson's disease and related synucleinopathies is a praiseworthy endeavor, but extremely challenging. Therapeutic candidates that were successful in preclinical Parkinson's disease animal models have repeatedly failed when tested in clinical trials. While these failures have many possible explanations, it is perhaps time to recognize that the problem lies with the animal models rather than the putative candidate.
View Article and Find Full Text PDFMotor modules are largely unaffected by pathological walking biomechanics: a simulation study.
J Neuroeng Rehabil
January 2025
Department of Mechanical and Aerospace Engineering, University of Florida, PO Box 116250, Gainesville, FL, 32611, USA.
Background: Motor module (a.k.a.
View Article and Find Full Text PDFLewy body diseases and the gut.
Mol Neurodegener
January 2025
Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, 20815, USA.
Gastrointestinal (GI) involvement in Lewy body diseases (LBDs) has been observed since the initial descriptions of patients by James Parkinson. Recent experimental and human observational studies raise the possibility that pathogenic alpha-synuclein (⍺-syn) might develop in the GI tract and subsequently spread to susceptible brain regions. The cellular and mechanistic origins of ⍺-syn propagation in disease are under intense investigation.
View Article and Find Full Text PDFToward a biological definition of neuronal and glial synucleinopathies.
Nat Med
January 2025
Department of Neurology & Neurological Sciences, Stanford Movement Disorders Center, Stanford University, Stanford, CA, USA.
Cerebral accumulation of alpha-synuclein (αSyn) aggregates is the hallmark event in a group of neurodegenerative diseases-collectively called synucleinopathies-which include Parkinson's disease, dementia with Lewy bodies and multiple system atrophy. Currently, these are diagnosed by their clinical symptoms and definitively confirmed postmortem by the presence of αSyn deposits in the brain. Here, we summarize the drawbacks of the current clinical definition of synucleinopathies and outline the rationale for moving toward an earlier, biology-anchored definition of these disorders, with or without the presence of clinical symptoms.
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