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Multiple Sclerosis: Glial Cell Diversity in Time and Space.
Glia
December 2024
Department of Neurology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Multiple sclerosis (MS) is the most prevalent human inflammatory disease of the central nervous system with demyelination and glial scar formation as pathological hallmarks. Glial cells are key drivers of lesion progression in MS with roles in both tissue damage and repair depending on the surrounding microenvironment and the functional state of the individual glial subtype. In this review, we describe recent developments in the context of glial cell diversity in MS summarizing key findings with respect to pathological and maladaptive functions related to disease-associated glial subtypes.
View Article and Find Full Text PDFGive us a hand, mate! A holistic review of research on human-machine teaming.
BMJ Mil Health
December 2024
University of Oxford Social Sciences Division, Oxford, UK.
Defence has a significant interest in the use of artificial intelligence (AI)-based technologies to address some of the challenges it faces. At the core of future military advantage will be the effective integration of humans and AI into human-machine teams (HMT) that leverages the capabilities of people and technologies to outperform adversaries. Realising the full potential of these technologies will depend on understanding the relative strengths of humans and machines, and how we design effective integration to optimise performance and resilience across all use cases and environments.
View Article and Find Full Text PDFStriatal-cortical dysconnectivity underlies somatosensory deficits in Parkinson's disease: Insights from rhythmic auditory-motor training.
Neurobiol Dis
December 2024
Graduate Institute of Brain and Mind Sciences, National Taiwan University College of Medicine, Taipei 10051, Taiwan. Electronic address:
Evidence indicates that neurodegenerative diseases spread through distinct brain networks. For Parkinson's disease (PD), somatosensory abnormalities may accompany motor dysfunction in early disease stages when dopaminergic degeneration is limited to the basal ganglia. It remains unclear whether, based on the network-spread account, these abnormalities emanated from aberrant functional connectivity with the basal ganglia, and whether interventions normalizing this connectivity could reverse these abnormalities.
View Article and Find Full Text PDFNext step towards functional precision medicine in neuro-oncology.
Neuro Oncol
December 2024
Department of Neurology, Clinical Neuroscience Center, University Hospital and University of Zurich, Zurich, Switzerland.
Synaptic dysfunction is one of the earliest cellular defects observed in Alzheimer's disease (AD) and Parkinson's disease (PD), occurring before widespread protein aggregation, neuronal loss, and cognitive decline. While the field has focused on the aggregation of Tau and α-Synuclein (α-Syn), emerging evidence suggests that these proteins may drive presynaptic pathology even before their aggregation. Therefore, understanding the mechanisms by which Tau and α-Syn affect presynaptic terminals offers an opportunity for developing innovative therapeutics aimed at preserving synapses and potentially halting neurodegeneration.
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