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C/EBPβ in Alzheimer's disease: An integrative regulator of pathological mechanisms.
Brain Res Bull
January 2025
Heilongjiang University of Traditional Chinese Medicine, Harbin, Heilongjiang, China.
Alzheimer's disease (AD) stands as one of the most prevalent neurodegenerative disorders, characterized by a progressive decline in cognitive function, neuroinflammation, amyloid-beta (Aβ) plaques, and neurofibrillary tangles (NFTs). With the global aging population, the incidence of AD continues to rise, yet current therapeutic strategies remain limited in their ability to significantly alleviate cognitive impairments. Therefore, a deeper understanding of the molecular mechanisms underlying AD is imperative for the development of more effective treatments.
View Article and Find Full Text PDFBiological Amyloids Chemically Damage DNA.
ACS Chem Neurosci
January 2025
Department of Life Sciences, Chalmers University of Technology, 412 96 Gothenburg, Sweden.
Amyloid fibrils are protein polymers noncovalently assembled through β-strands arranged in a cross-β structure. Biological amyloids were considered chemically inert until we and others recently demonstrated their ability to catalyze chemical reactions in vitro. To further explore the functional repertoire of amyloids, we here probe if fibrils of α-synuclein (αS) display chemical reactivity toward DNA.
View Article and Find Full Text PDFMass Spectrometry-Based Protein Footprinting for Protein Structure Characterization.
Acc Chem Res
January 2025
Department of Chemistry, Washington University, St. Louis, Missouri 63130, United States.
ConspectusProtein higher-order structure (HOS) is key to biological function because the mechanisms of protein machinery are encoded in protein three-dimensional structures. Mass spectrometry (MS)-based protein footprinting is advancing protein structure characterization by mapping solvent-accessible regions of proteins and changes in H-bonding, thereby providing higher order structural information. Footprinting provides insights into protein dynamics, conformational changes, and interactions, and when conducted in a differential way, can readily reveal those regions that undergo conformational change in response to perturbations such as ligand binding, mutation, thermal stress, or aggregation.
View Article and Find Full Text PDFAPP lysine 612 lactylation ameliorates amyloid pathology and memory decline in Alzheimer's disease.
J Clin Invest
January 2025
Growth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, China.
Article Synopsis
- Posttranslational modification (PTM) of the amyloid precursor protein (APP), particularly lactylation, is linked to the development of Alzheimer's disease (AD), but its specific role is still unclear.
- Research showed reduced APP lactylation in AD patients and models, identifying lysine 612 as a key lactylation site, which affects APP processing and Aβ generation.
- A lactyl-mimicking mutant enhanced APP trafficking and reduced cognitive decline by modifying APP interactions, suggesting that targeting APP lactylation may offer new therapeutic avenues for Alzheimer's disease.
Alzheimer's disease: a comprehensive review of epidemiology, risk factors, symptoms diagnosis, management, caregiving, advanced treatments and associated challenges.
Front Med (Lausanne)
December 2024
Social Determinants of Health Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Background: Alzheimer's disease (AD) is a chronic, progressive neurodegenerative disorder characterized by cognitive decline, memory loss, and impaired reasoning. It is the leading cause of dementia in older adults, marked by the pathological accumulation of amyloid-beta plaques and neurofibrillary tangles. These pathological changes lead to widespread neuronal damage, significantly impacting daily functioning and quality of life.
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