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http://dx.doi.org/10.1016/0006-8993(71)90526-9 | DOI Listing |
CNS Drugs
January 2025
Cornwall Intellectual Disability Equitable Research (CIDER), University of Plymouth, Truro, England.
There is a synergistic relationship between epilepsy and intellectual disability (ID), and the approach to managing people with these conditions needs to be holistic. Epilepsy is the main co-morbidity associated with ID, and clinical presentation tends to be complex, associated with higher rates of treatment resistance, multi-morbidity and premature mortality. Despite this relationship, there is limited level 1 evidence to inform treatment choice for this vulnerable population.
View Article and Find Full Text PDFAging Clin Exp Res
January 2025
Instituto de Neurociencias del Principado de Asturias (INEUROPA), University of Oviedo, Oviedo, 33003, Spain.
Background: The presence of frailty is common in people with Parkinson's disease, as is cognitive dysfunction. Previous research on frailty has focused on the physical aspects of the pathology.
Aims: To analyze the relationship between frailty and cognitive impairment in patients with Parkinson's disease and to know which disease characteristics are associated with frailty.
Alzheimers Dement
December 2024
Allen Institute for Brain Science, Seattle, WA, USA.
Background: Applying single-cell RNA sequencing (scRNA-seq) to the study of neurodegenerative disease has propelled the field towards a more refined cellular understanding of Alzheimer's disease (AD); however, directly linking protein pathology to transcriptomic changes has not been possible at scale. Recently, a high-throughput method was developed to generate high-quality scRNA-seq data while retaining cytoplasmic proteins. Tau is a cytoplasmic protein and when hyperphosphorylated is integrally involved in AD progression.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
Background: Progressive supranuclear palsy (PSP) is a neurodegenerative disorder involving pathological deposition of tau that includes glial inclusions and specific regional vulnerability patterns. Therapeutic developments are hampered by incomplete understanding of disease mechanisms. Few studies have examined its cell type-specific effects.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Cell Biology and Pathology, New York, NY, USA.
Background: Possession of the APOE4 allele is the strongest genetic risk factor for developing the sporadic form of Alzheimer's disease (AD). Studies investigating APOE4's associated AD risk have largely centered on APOE4's propensity to regulate the deposition of extracellular amyloid beta plaques. More recent attempts to characterize APOE4's role in AD have brought into question the role APOE4 may possess in modulating the pathogenesis of intracellular tau tangles.
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