Four rhesus monkey pituitary glands were examined by transmission electron microscopy. Three types of intercellular junctions, desmosomes, hemidesmosomes and zonula adherens-type junctions, were observed between adjacent granular cells, folliculo-stellate cells, and joining a folliculo-stellate cell with a granular cell. Demosomes were most commonly observed between granular cells while the zonula adherens-type junctions were generally found between the folliculo-stellate cells.
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http://dx.doi.org/10.1002/ar.1091950101 | DOI Listing |
Alzheimers Dement
December 2024
Institut de recherches cliniques de Montréal (IRCM), Montréal, QC, Canada.
Background: Soluble Aβ oligomers (AβOs) induce synapse dysfunction, leading to cognitive impairment and memory deficits in Alzheimer's disease (AD). Our laboratory and several research groups characterized neurexin family members' physiological roles, pivotal synaptic adhesion molecules for development, plasticity, and maintenance. Beyond their normal functions, we found neurexins binding to AβOs causes AβO-induced neurexin dysregulation.
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December 2024
Salk Institute for Biological Studies, La Jolla, CA, USA.
Background: As humans age, some experience cognitive impairment while others do not. When impairment occurs, it varies in severity across individuals. Translationally relevant models are critical for understanding the neurobiological drivers of this variability, which is essential to uncovering the mechanisms underlying the brain's susceptibility to aging.
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December 2024
Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Background: Clinicopathological studies of Alzheimer's disease (AD) have demonstrated that synaptic or neuronal loss and clinical cognitive decline do not reliably correlate with fibrillar amyloid burden. We created a transgenic mouse model overexpressing Dutch (E693Q) mutant human amyloid precursor protein (APP) driven by the pan-neuronal Thy1 promoter. Accumulation of APP carboxyl-terminal fragments was observed in the brains of these mice, which develop an impaired learning phenotype directly proportional to brain oAβ levels.
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December 2024
Univ. Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167-RID-AGE, DISTALZ, Lille, France.
Background: BIN1 is a major susceptibility gene for AD and BIN1 protein interacts with Tau. However, the contribution of BIN1 and its isoforms to AD pathogenesis remains unclear. We recently described that human BIN1 isoform1 (BIN1iso1) induces an accumulation of early endosome vesicles leading to neurodegeneration in Drosophila retina and that the early endosome size regulation was conserved in human induced neurons.
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December 2024
Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil.
Background: The proteasome plays key roles in synaptic plasticity and memory by regulating protein turnover, quality control, and elimination of oxidized/misfolded proteins. Here, we investigate proteasome function and localization at synapses in Alzheimer's disease (AD) post-mortem brain tissue and in experimental models.
Method: We used primary hippocampal cultures, amyloid-β oligomers (AβO)-injected or transgenic animal models, and human brain tissue to determine brain proteasome function and subcellular localization.
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