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Aim: In clinical practice, cardiologists frequently note substantial differences in coronary artery health among patients of the same age bracket. This observation led to our investigation into identifying genes that are shared between atherosclerosis and aging, as well as those that are specifically amplified in atherosclerosis alone.

Methods: Our study leveraged existing gene expression datasets from the Gene Expression Omnibus (GEO), avoiding the need for new experimental research involving human or animal subjects.

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In Alzheimer's disease (AD), tau dissociates from microtubules (MTs) due to hyperphosphorylation and misfolding. It is degraded by various mechanisms, including the 20S proteasome, chaperone-mediated autophagy (CMA), 26S proteasome, macroautophagy, and aggrephagy. Neurofibrillary tangles (NFTs) form upon the impairment of aggrephagy, and eventually, the ubiquitin chaperone valosin-containing protein (VCP) and heat shock 70 kDa protein (HSP70) are recruited to the sites of NFTs for the extraction of tau for the ubiquitin-proteasome system (UPS)-mediated degradation.

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Article Synopsis
  • Clinical trials targeting a specific molecular pathway have been ineffective in treating Alzheimer's disease, highlighting the need to address the effects of Aβ protein aggregation and neuroinflammation.
  • Researchers designed a nano-sized flower mesoporous selenium carrier that delivers metformin (a diabetes drug) to the brain by targeting transferrin receptors, facilitating transport across the blood-brain barrier.
  • In animal models, this system not only released metformin effectively at the site of Alzheimer's lesions but also promoted neuroprotection and improved cognitive function by reducing Aβ deposits and enhancing microglial activity.
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Apoptosis is a genetically programmed form of cell death that is substantially conserved across the evolutionary tree. Apoptotic cell elimination includes recognition, phagocytosis, and degradation. Failure to clear apoptotic cells can ultimately cause a series of human diseases, such as systemic lupus erythematosus, Alzheimer's disease, atherosclerosis, and cancer.

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Oligodendrocyte precursor cells (OPCs) sculpt neural circuits through the phagocytic engulfment of synapses during development and adulthood. However, existing techniques for analyzing synapse engulfment by OPCs have limited accuracy. Here we describe the quantification of synapse engulfment by OPCs via a two-pronged cell biological approach that combines high-confidence and high-throughput methodologies.

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