We report the developmental neuropathology for rat pups at postnatal day (PND) 37 and PND 77 and the molecular biomarkers for PND 35, 75, and 350 after perinatal exposure to a reconstituted mixture of persistent organochlorine pollutants (POPs) based on the blood profiles of people living in the Great Lake Basin. The developmental neuropathology included routine histopathology evaluation, quantification of cell proliferation and death in the subventricular zone, linear morphometric measurements, and transcriptional analysis. No histopathological, structural, or stereological changes were observed in animals treated with the POPs or Aroclor 1254, on PND 37 or PND 77. While no transcriptional changes were found in Arcolor-treated animals, significant transcriptional changes were observed on PND 350 in female offspring perinatally exposed to 0.13 mg/kg of the POP mixture. Markers of the cholinergic system including acetylcholinesterase and the muscarinic receptors (subtypes M1-M5) were downregulated 2- to 6-fold. In addition, structural genes including neurofilaments (NFLs) and microtubule-associated protein (MAP-2) were downregulated at least 2-fold or greater. Our results support that in utero and lactational exposure to the chemical mixture of POPs lead to developmental changes in adult rat brains.
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Nat Commun
January 2025
Institute of Developmental Biology and Neurobiology, Faculty of Biology, Johannes Gutenberg University Mainz, Mainz, Germany.
After a peripheral nerve injury, Schwann cells (SCs), the myelinating glia of the peripheral nervous system, convert into repair cells that foster axonal regrowth, and then remyelinate or re-ensheath regenerated axons, thereby ensuring functional recovery. The efficiency of this mechanism depends however on the time needed for axons to regrow. Here, we show that ablation of histone deacetylase 8 (HDAC8) in SCs accelerates the regrowth of sensory axons and sensory function recovery.
View Article and Find Full Text PDFNeurooncol Adv
December 2024
Developmental Therapeutics and Pharmacology Unit, Surgical Neurology Branch, National Institute of Neurologic Disorders and Stroke (NINDS), NIH, Bethesda, Maryland 20892, USA.
Background: Survival of pediatric and young adults with malignant glioma remains poor despite progress in treatment. This is especially true for diffuse hemispheric glioma (DHG), H3 G34-mutant, which is often present in adolescent and young adult patients. This scoping review consolidates existing knowledge of DHG H3 G34-mutant and identifies future targets and therapeutic options.
View Article and Find Full Text PDFNat Genet
January 2025
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Ontario, Canada.
Transcription factors are frequent cancer driver genes, exhibiting noted specificity based on the precise cell of origin. We demonstrate that ZIC1 exhibits loss-of-function (LOF) somatic events in group 4 (G4) medulloblastoma through recurrent point mutations, subchromosomal deletions and mono-allelic epigenetic repression (60% of G4 medulloblastoma). In contrast, highly similar SHH medulloblastoma exhibits distinct and diametrically opposed gain-of-function mutations and copy number gains (20% of SHH medulloblastoma).
View Article and Find Full Text PDFSci Rep
December 2024
Institute of Psychology, University of Bern, Bern, Switzerland.
Aging is typically associated with declines in episodic memory, executive functions, and sleep quality. Therefore, the sleep-dependent stabilization of episodic memory is suspected to decline during aging. This might reflect in accelerated long-term forgetting, which refers to normal learning and retention over hours, yet an abnormal retention over nights and days.
View Article and Find Full Text PDFFront Neural Circuits
December 2024
Department of Cellular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan.
Our brain adapts to the environment by optimizing its function through experience-dependent cortical plasticity. This plasticity is transiently enhanced during a developmental stage, known as the "critical period," and subsequently maintained at lower levels throughout adulthood. Thus, understanding the mechanism underlying critical period plasticity is crucial for improving brain adaptability across the lifespan.
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