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Geriatr Gerontol Int
January 2025
Department of Cardiology, National Center for Geriatrics and Gerontology, Obu, Japan.
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.
Int J Mol Sci
November 2024
Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
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.
View Article and Find Full Text PDFColloids Surf B Biointerfaces
January 2025
Shenzhen Longhua Maternity and Child Healthcare Hospital, Shenzhen 518110, China. Electronic address:
FASEB Bioadv
September 2024
College of Life Sciences, Shaanxi Normal University Xi'an China.
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.
View Article and Find Full Text PDFNat Protoc
October 2024
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
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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