The pH 5 supernatant fractions prepared from homogenates of tissues of normal and dystrophic mice were used to study the incorporation of [14C]phenylalanyl-tRNA into peptide. The incorpoation was markedly reduced using the muscle pH 5 supernatant fraction from dystrophic animals but no reduction was seen with brain, liver or heart preparations from dystrophic mice. The lower incorporation with dystrophic muscle pH 5 supernatant was not due to altered activity of ribonuclease, elongation factors, proteolytic enzymes, GTP or sulfhydryl reagents, but was attributable to the presence of activity that was inhibitory to protein synthesis.
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http://dx.doi.org/10.1016/0005-2787(76)90204-5 | DOI Listing |
Alzheimers Dement
December 2024
Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Background: Accumulation of the amyloid-β (Aβ) peptide into amyloid plaque is one of the key pathological markers of Alzheimer's disease (AD). Apolipoprotein E (APOE) is known to modify AD risk and has been reported to influence Aβ accumulation in the brain in an isoform-dependent manner. ApoE can be produced by various cell types in the brain, with astrocytes being the main producer.
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December 2024
Institute of Brain Sciene, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Background: Genome-wide association studies demonstrated that immune suppressive receptor CD33 variants are associated with high susceptibility to developing Alzheimer's disease (AD). Human CD33 (hCD33) regulates microglial immune response and clearance ability. However, the differential regulation of phagocytosis by human and mouse CD33 imposes constraints on utilizing the mouse model for investigating the role of CD33 in AD.
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December 2024
University of California, Irvine, Irvine, CA, USA.
Background: Condensed extracellular matrix structures called perineuronal nets (PNNs) preferentially enwrap the soma and stabilize proximal synapses of parvalbumin-expressing inhibitory neurons in the cortex, serving as a protective barrier against neurotoxins. While PNN structural integrity declines in the healthy aging brain, this reduction is exacerbated in Alzheimer's disease (AD). In the 5xFAD mouse model of amyloidosis, the elimination of microglia prevents reductions in PNN, suggesting microglia are responsible for the over-degradation of PNNs observed in AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Background: Plaques are a hallmark feature of Alzheimer's disease (AD). We found the loss of mucosal-associated invariant T (MAIT) cells and its antigen-presenting molecule MR1 caused a delay in plaque pathology development in AD mouse models. However, it remains unknown how this axis is impacting microglial response and dystrophic neurites.
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