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Development and application of a clinical core data set for deep brain stimulation in Parkinson's disease, dystonia or tremor: from data collection to data exchange and data sharing.
Neurol Res Pract
January 2025
Institute of Clinical Epidemiology and Biometry, Julius-Maximilians-Universität Würzburg (JMU), Haus D7, Josef-Schneider-Straße 2, 97080, Würzburg, Germany.
Background: Comprehensive clinical data regarding factors influencing the individual disease course of patients with movement disorders treated with deep brain stimulation might help to better understand disease progression and to develop individualized treatment approaches.
Methods: The clinical core data set was developed by a multidisciplinary working group within the German transregional collaborative research network ReTune. The development followed standardized methodology comprising review of available evidence, a consensus process and performance of the first phase of the study.
Clinical perspective on pluripotent stem cells derived cell therapies for the treatment of neurodegenerative diseases.
Adv Drug Deliv Rev
January 2025
Neurodegenerative Diseases Department, Kadimastem Ltd, Pinchas Sapir 7, Weizmann Science Park, Ness-Ziona, Israel; Department of Molecular Genetics, Weizmann Institute of Science, 76100, Rehovot, Israel.
Self-renewal capacity and potential to differentiate into almost any cell type of the human body makes pluripotent stem cells a valuable starting material for manufacturing of clinical grade cell therapies. Neurodegenerative diseases are characterized by gradual loss of structure or function of neurons, often leading to neuronal death. This results in gradual decline of cognitive, motor, and physiological functions due to the degeneration of the central nervous systems.
View Article and Find Full Text PDFExecutive dysfunction in Parkinson's disease: From neurochemistry to circuits, genetics and neuroimaging.
Prog Neuropsychopharmacol Biol Psychiatry
January 2025
Department of Rehabilitation, Yantai Yuhuangding Hospital, Qingdao University, Yantai, China; Department of Neurology, Yantai Yuhuangding Hospital, Qingdao University, Yantai, China; Department of Clinical Medical Research Center, Yantai Yuhuangding Hospital, Qingdao University, Yantai, China. Electronic address:
Cognitive decline is one of the most significant non-motor symptoms of Parkinson's disease (PD), with executive dysfunction (EDF) being the most prominent characteristic of PD-associated cognitive deficits. Currently, lack of uniformity in the conceptualization and assessment scales for executive functions impedes the early and accurate diagnosis of executive dysfunction in PD. The neurobiological mechanisms of executive dysfunction in PD remain poorly understood.
View Article and Find Full Text PDFCommon alterations to astrocytes across neurodegenerative disorders.
Curr Opin Neurobiol
January 2025
Salk Institute for Biological Studies, Molecular Neurobiology Laboratory, 10010 North Torrey Pines Rd, La Jolla, CA, 92037, USA. Electronic address:
Astrocytes perform multiple functions in the nervous system, many of which are altered in neurodegenerative disorders. In this review, we explore shared astrocytic alterations across neurodegenerative disorders, including Alzheimer's disease, Huntington's disease, Parkinson's disease, amyotrophic lateral sclerosis, and frontotemporal lobe degeneration. Assessing recent datasets of single-nucleus RNA-sequencing of human brains, a theme emerges of common alterations in astrocyte state across disorders including in neuroinflammation, synaptic organization, metabolic support, and the cellular stress response.
View Article and Find Full Text PDFaux orchestrates the phosphorylation-dependent assembly of the lysosomal V-ATPase in glia and contributes to SNCA/α-synuclein degradation.
Autophagy
January 2025
School of Life Science and Technology, ShanghaiTech University, Shanghai, China.
Glia contribute to the neuropathology of Parkinson disease (PD), but how they react opposingly to be beneficial or detrimental under pathological conditions, like promoting or eliminating SNCA/α-syn (synuclein alpha) inclusions, remains elusive. Here we present evidence that aux (auxilin), the homolog of the PD risk factor GAK (cyclin G associated kinase), regulates the lysosomal degradation of SNCA/α-syn in glia. Lack of glial GAK/aux increases the lysosome number and size, regulates lysosomal acidification and hydrolase activity, and ultimately blocks the degradation of substrates including SNCA/α-syn.
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