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Assessing Human Ribosomal DNA Variation and Its Association With Phenotypic Outcomes.
Bioessays
January 2025
The Blizard Institute, School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Although genome-scale analyses have provided insights into the connection between genetic variability and complex human phenotypes, much trait variation is still not fully understood. Genetic variation within repetitive elements, such as the multi-copy, multi-locus ribosomal DNA (rDNA), has emerged as a potential contributor to trait variation. Whereas rDNA was long believed to be largely uniform within a species, recent studies have revealed substantial variability in the locus, both within and across individuals.
View Article and Find Full Text PDFVenous compression causes chronic cerebral ischaemia in normal pressure hydrocephalus patients.
Fluids Barriers CNS
January 2025
Department of Neurosurgery, Osaka Medical and Pharmaceutical University, Takatsuki, Osaka, Japan.
Background: Cerebral autoregulation is a robust regulatory mechanism that stabilizes cerebral blood flow in response to reduced blood pressure, thereby preventing cerebral ischaemia. Scientists have long believed that cerebral autoregulation also stabilizes cerebral blood flow against increases in intracranial pressure, which is another component that determines cerebral perfusion pressure. However, this idea was inconsistent with the complex pathogenesis of normal pressure hydrocephalus, which includes components of chronic cerebral ischaemia due to mild increases in intracranial pressure.
View Article and Find Full Text PDFA revised view of the role of CaMKII in learning and memory.
Nat Neurosci
January 2025
Department of Basic and Clinical Neuroscience, King's College London, London, UK.
The Ca/calmodulin (CaM)-dependent protein kinase II (CaMKII) plays a fundamental role in learning and possibly also in memory. However, current mechanistic models require fundamental revision. CaMKII autophosphorylation at Thr286 (pThr286) does not provide the molecular basis for long-term memory, as long believed.
View Article and Find Full Text PDFUnlabelled: Neuronal hyperexcitability is a hallmark of amyotrophic lateral sclerosis (ALS) but its relationship with the TDP-43 aggregates that comprise the predominant pathology in over 90% of ALS cases remains unclear. Emerging evidence in tissue and slice culture models indicate that TDP-43 pathology induces neuronal hyperexcitability suggesting it may be responsible for the excitotoxicity long believed to be a major driver of ALS neuron death. Here, we characterized hyperexcitability and neurodegeneration in the hippocampus of doxycycline-regulatable rNLS8 mice (NEFH-tTA x tetO-hTDP-43ΔNLS), followed by treatment with AAV encoded DREADDs and anti-seizure medications to measure the effect on behavioral function and neurodegeneration.
View Article and Find Full Text PDFArticle Synopsis
- Hematopoietic stem cells are influenced by their surrounding niche of endothelial and mesenchymal stromal cells in bone marrow, which plays a crucial role in leukemia development.
- Researchers discovered that leukemic cells release a peptide called apelin, which causes changes in the niche cells that promote the progression of leukemia.
- Blocking apelin in leukemic zebrafish showed a reduction in disease symptoms, suggesting that targeting apelin could be a promising new treatment approach for leukemia.
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