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| http://dx.doi.org/10.26599/1671-5411.2023.06.007 | DOI Listing |
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Alzheimers Dement
December 2024
Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Background: Despite age being the primary risk factor for Alzheimer's disease (AD), there remains a necessity for a thorough understanding of the distinct biological pathways affected in the course of healthy aging as opposed to the pathological aging that leads to neurodegeneration. As the genome remains constant throughout one's lifespan, it becomes crucial to unravel the impact of aging on the proteome. Proteins, being key players in various cellular functions, mediate the effects of environmental stimuli and epigenetic alterations.
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Alzheimers Dement
December 2024
University of São Paulo Universidade de São Paulo, São Paulo, Brazil.
Background: The Down Syndrome (DS), also referred to as trisomy of chromosome 21, is a prevalent cause of intellectual disability and also contributes to the acceleration of aging, among other developmental and health concerns. Certain pathological characteristics shared by DS and Alzheimer's Disease (AD) indicate similar commonalities. This study aims to unravel the relationship between the canonical Wnt/pathway, the amyloid precursor protein processing, the telomere shortening in DS individuals.
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Alzheimers Dement
December 2024
Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Background: The present study delves into the intricate molecular connections between ischemic stroke (IS) and Alzheimer's disease (AD) through an analysis of mitochondrial microRNA (miRNA) patterns. By exploring their shared signatures in the context of IS and AD, our aim is to unravel potential common pathways, understand shared molecular mechanisms, explore diagnostic and therapeutic opportunities, gain a comprehensive understanding of neurodegeneration, and advance the field of biomarker research.
Method: To explore these intriguing questions, mitochondria were isolated from postmortem brains of individuals with IS, AD, and healthy controls (n=10 each).
Solvent-Driven Self-Assembly of Discrete Ni(II)-Azide Complexes: Unraveling Unusual Behavior in Mimicking Jack Bean Urease.
Inorg Chem
January 2025
Department of Chemistry, University College of Science, University of Calcutta, 92 A.P.C. Road, Kolkata 700009, India.
The well-known inhibitory strength of 3d metal Schiff base complexes against urease enzymes has long been acknowledged, but their untapped potential to act as ureolytic mimics of active metallobiosites remained unexplored. To break the new ground, we present pyrrolidine-based mononuclear Ni(II)-azide complex {[NiL(HL)(N)]·1.5(HO)} using the N,N,O donor ligand, namely ()-4-bromo-2-(((2-(pyrrolidin-1-yl)ethyl)imino)methyl)phenol.
View Article and Find Full Text PDFAutophagy intersection: Unraveling the role of the SNARE complex in lysosomal fusion in Alzheimer's disease.
J Alzheimers Dis
January 2025
School of Medicine, Chongqing University, Chongqing, P.R. China.
Autophagy is a fundamental cellular process critical for maintaining neuronal health, particularly in the context of neurodegenerative diseases such as Alzheimer's disease (AD). This review explores the intricate role of the SNARE complex in the fusion of autophagosomes with lysosomes, a crucial step in autophagic flux. Disruptions in this fusion process, often resulting from aberrant SNARE complex function or impaired lysosomal acidification, contribute to the pathological accumulation of autophagosomes and lysosomes observed in AD.
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