An ultrastructural study of changes in synaptic contacts and astrocytic processes of postmortem hippocampus was performed in 5 cases of Alzheimer's disease. Mossy fibres in the stratum lucidum were examined. Pronounced alterations included clustering of synaptic vesicles, membranous damage and multilamellar profiles in synaptic terminals. There were many hypertrophic astrocytic processes around synapses. The findings suggest that the ultrastructural alterations in mossy fibers expansion, and the disturbance of glio-synaptic relationships might contribute to memory impairment in Alzheimer's disease.
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Mol Psychiatry
January 2025
Institut de Neurociències, Department de Bioquímica i Biologia Molecular, Facultat de Medicina, Universitat Autònoma de Barcelona, Bellaterra, Barcelona, Spain.
Alzheimer's disease (AD) is characterized by memory loss and neuropsychiatric symptoms associated with cerebral amyloid-β (Aβ) and tau pathologies, but whether and how these factors differentially disrupt neural circuits remains unclear. Here, we investigated the vulnerability of memory and emotional circuits to Aβ and tau pathologies in mice expressing mutant human amyloid precursor protein (APP), Tau or both APP/Tau in excitatory neurons. APP/Tau mice develop age- and sex-dependent Aβ and phosphorylated tau pathologies, the latter exacerbated at early stages, in vulnerable brain regions.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran.
In recent decades, researchers and clinicians have increasingly focused on glial cell function. One of the primary mechanisms influencing these functions is through extracellular vesicles (EVs), membrane-bound particles released by cells that are essential for intercellular communication. EVs can be broadly categorized into four main types based on their size, origin, and biogenesis: large EVs, small EVs (sEVs), autophagic EVs, and apoptotic bodies.
View Article and Find Full Text PDFBMC Pharmacol Toxicol
January 2025
Department of Anatomy, College of Health Sciences, University of Ilorin, Ilorin, 240003, Nigeria.
Background: Glia mediated neuroinflammation and degeneration of inhibitory GABAergic interneurons are some of the hall marks of pyrethroid neurotoxicity. Here we investigated the sex specific responses of inflammatory cytokines, microglia, astrocyte and parvalbumin positive inhibitory GABAergic interneurons to λ-cyhalothrin (LCT) exposures in rats.
Methods: Equal numbers of male and female rats were given oral corn oil, 2 mg/kg.
Front Cell Neurosci
January 2025
School of Veterinary Medicine, Institute of Pharmacology and Toxicology, Freie Universität Berlin, Berlin, Germany.
Infections impacting the central nervous system (CNS) constitute a substantial predisposing factor for the emergence of epileptic seizures. Given that epilepsy conventionally correlates with hippocampal sclerosis and neuronal degeneration, a potentially innovative avenue for therapeutic intervention involves fostering adult neurogenesis, a process primarily occurring within the subgranular zone of the dentate gyrus (DG) through the differentiation of neural stem cells (NSC). While experimental seizures induced by chemoconvulsants or electrical stimulation transiently enhance neurogenesis, the effects of encephalitis and the resultant virus-induced seizures remain inadequately understood.
View Article and Find Full Text PDFAlzheimers Res Ther
January 2025
Translational Neurodegeneration Research and Neuropathology Lab, Department of Clinical Medicine (KlinMed), Medical Faculty, University of Oslo (UiO) and Section of Neuropathology Research, Department of Pathology (PAT), Clinics for Laboratory Medicine (KLM), Oslo University Hospital (OUS), Sognsvannsveien 20, Oslo, NO-0372, Norway.
Background: Specific genetic variants in the ATP-binding cassette transporter A7 locus (ABCA7) are associated with an increased risk of Alzheimer's disease (AD). ABCA7 transports lipids from/across cell membranes, regulates Aβ peptide processing and clearance, and modulates microglial and T-cell functions to maintain immune homeostasis in the brain. During AD pathogenesis, neuroinflammation is one of the key mechanisms involved.
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