The connection between body weight alterations and Alzheimer's disease highlights the intricate relationship between the brain and adipose tissue in the context of neurological disorders. During midlife, weight gain increases the risk of cognitive decline and dementia, whereas in late life, weight gain becomes a protective factor. Despite their substantial impact on metabolism, the role of adipokines in the transition from healthy aging to neurological disorders remains largely unexplored. We aim to investigate how the adipose tissue milieu and the secreted adipokines are involved in the transition between biological and pathological aging, highlighting the bidirectional relationship between the brain and systemic metabolism. Understanding the function of these adipokines will allow us to identify biomarkers for early detection of Alzheimer's disease and uncover novel therapeutic options.
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http://dx.doi.org/10.3390/ijms25115932 | DOI Listing |
Sci Adv
January 2025
Department of Biostatistics and Health Data Science, School of Medicine, Indiana University, Indianapolis, IN 46202, USA.
Alzheimer's disease (AD) is the leading dementia among the elderly with complex origins. Despite extensive investigation into the AD-associated protein-coding genes, the involvement of noncoding RNAs (ncRNAs) and posttranscriptional modification (PTM) in AD pathogenesis remains unclear. Here, we comprehensively characterized the landscape of ncRNAs and PTM events in 1460 samples across six brain regions sourced from the Mount Sinai/JJ Peters VA Medical Center Brain Bank Study and Mayo cohorts, encompassing 33,321 long ncRNAs, 92,897 enhancer RNAs, 53,763 alternative polyadenylation events, and 900,221 A-to-I RNA editing events.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Anesthesiology & Perioperative Medicine, University of Rochester, Rochester, New York, United States of America.
Neurodegenerative diseases are often characterized by mitochondrial dysfunction. In Alzheimer's disease, abnormal tau phosphorylation disrupts mitophagy, a quality control process through which damaged organelles are selectively removed from the mitochondrial network. The precise mechanism through which this occurs remains unclear.
View Article and Find Full Text PDFJAMA Netw Open
January 2025
Department of Health Policy and Management, Yale School of Public Health, New Haven, Connecticut.
Importance: Disparities in cognition, including dementia occurrence, persist between non-Hispanic Black (hereinafter, Black) and non-Hispanic White (hereinafter, White) older adults, and are possibly influenced by early educational differences stemming from structural racism. However, the association between school racial segregation and later-life cognition remains underexplored.
Objective: To investigate the association between childhood contextual exposure to school racial segregation and cognitive outcomes in later life.
Neuromolecular Med
December 2024
Key Laboratory of Physical Fitness and Exercise Rehabilitation of Hunan Province, College of Physical Education, Hunan Normal University, Changsha, 410012, China.
Alzheimer's disease (AD) is the most common neurodegenerative disorder. The neuropathology of AD appears in the hippocampus. The purpose of this work was to reveal key differentially expressed genes (DEGs) in the hippocampus of AD patients and healthy individuals.
View Article and Find Full Text PDFInflammopharmacology
January 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, ElKasr Elaini Street, Cairo, 11562, Egypt.
The currently approved drugs for Alzheimer's disease (AD) are only for symptomatic treatment in the early stages of the disease but they could not halt the neurodegeneration, additionally, the safety profile of the recently developed immunotherapy is a big issue. This review aims to explain the importance of the drugs repurposing technique and strategy to develop therapy for AD. We illustrated the biological alterations in the pathophysiology of AD including the amyloid pathology, the Tau pathology, oxidative stress, mitochondrial dysfunction, neuroinflammation, glutamate-mediated excitotoxicity, insulin signaling impairment, wingless-related integration site/β-catenin signaling, and autophagy.
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