Red blood cell distribution width to albumin ratio (RAR) is associated with low cognitive performance in American older adults: NHANES 2011–2014

BMC Geriatrics, Journal Year: 2025, Volume and Issue: 25(1)

Published: March 7, 2025

The red blood cell distribution width to albumin ratio (RAR) is a novel comprehensive biomarker of inflammation and nutrition, which has emerged as reliable prognostic indicator for adverse outcomes mortality in patients with various diseases. However, the association between RAR low cognitive performance older adults remains unclear. This study aims investigate relationship among United States. study, retrospective analysis, included 2,765 participants aged 60 years from National Health Nutrition Examination Survey (NHANES) conducted 2011 2014. Low was assessed using word learning subset Consortium Establish Registry Alzheimer's Disease (CERAD), Digit Symbol Substitution Test (DSST), Animal Fluency (AFT). defined scores below lowest quartile each test. evaluated weighted multivariable logistic regression, restricted cubic splines (RCS), subgroup analyses. After adjusting all potential confounders, independently linearly positively associated both DSST AFT performance. Specifically, compared first RAR, those fourth had adjusted ORs (95% CIs) 1.81 (1.03, 3.20) 1.68 (1.05, 2.67) Subgroup analysis did not reveal significant interactions stratification variables. significantly Maintaining lower may be crucial strategy mitigating risk decline elderly population.

Language: Английский

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Decoding microglial immunometabolism: a new frontier in Alzheimer's disease research

Molecular Neurodegeneration, Journal Year: 2025, Volume and Issue: 20(1)

Published: March 27, 2025

Abstract Alzheimer’s disease (AD) involves a dynamic interaction between neuroinflammation and metabolic dysregulation, where microglia play central role. These immune cells undergo reprogramming in response to AD-related pathology, with key genes such as TREM2, APOE, HIF-1α orchestrating these processes. Microglial metabolism adapts environmental stimuli, shifting oxidative phosphorylation glycolysis. Hexokinase-2 facilitates glycolytic flux, while AMPK acts an energy sensor, coordinating lipid glucose metabolism. TREM2 APOE regulate microglial homeostasis, influencing Aβ clearance responses. LPL ABCA7, both associated AD risk, modulate processing cholesterol transport, linking neurodegeneration. PPARG further supports by regulating inflammatory Amino acid also contributes function. Indoleamine 2,3-dioxygenase controls the kynurenine pathway, producing neurotoxic metabolites linked pathology. Additionally, glucose-6-phosphate dehydrogenase regulates pentose phosphate maintaining redox balance activation. Dysregulated metabolism, influenced genetic variants APOE4, impair responses exacerbate progression. Recent findings highlight interplay regulators like REV-ERBα, which modulates inflammation, Syk, influences clearance. insights offer promising therapeutic targets, including strategies aimed at modulation, could restore function depending on stage. By integrating metabolic, immune, factors, this review underscores importance of immunometabolism AD. Targeting pathways provide novel for mitigating restoring function, ultimately paving way innovative treatments neurodegenerative diseases.

Language: Английский

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Decoding Neurodegeneration: A Review of Molecular Mechanisms and Therapeutic Advances in Alzheimer’s, Parkinson’s, and ALS

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 12613 - 12613

Published: Nov. 24, 2024

Neurodegenerative diseases, such as Alzheimer's, Parkinson's, ALS, and Huntington's, remain formidable challenges in medicine, with their relentless progression limited therapeutic options. These diseases arise from a web of molecular disturbances-misfolded proteins, chronic neuroinflammation, mitochondrial dysfunction, genetic mutations-that slowly dismantle neuronal integrity. Yet, recent scientific breakthroughs are opening new paths to intervene these once-intractable conditions. This review synthesizes the latest insights into underlying dynamics neurodegeneration, revealing how intertwined pathways drive course diseases. With an eye on most promising advances, we explore innovative therapies emerging cutting-edge research: nanotechnology-based drug delivery systems capable navigating blood-brain barrier, gene-editing tools like CRISPR designed correct harmful variants, stem cell strategies that not only replace lost neurons but foster neuroprotective environments. Pharmacogenomics is reshaping treatment personalization, enabling tailored align individual profiles, while diagnostics biomarkers ushering era early, precise disease detection. Furthermore, novel perspectives gut-brain axis sparking interest mounting evidence suggests microbiome modulation may play role reducing neuroinflammatory responses linked neurodegenerative progression. Taken together, advances signal shift toward comprehensive, personalized approach could transform care. By integrating techniques, this offers forward-looking perspective future where treatments aim just manage symptoms fundamentally alter progression, presenting renewed hope for improved patient outcomes.

Language: Английский

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Alzheimer’s disease and diabetes-associated cognitive dysfunction: the microglia link?

Metabolic Brain Disease, Journal Year: 2025, Volume and Issue: 40(1)

Published: Jan. 4, 2025

Language: Английский

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Targeting Ferroptosis in Parkinson’s: Repurposing Diabetes Drugs as a Promising Treatment

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(4), P. 1516 - 1516

Published: Feb. 11, 2025

This review explores the promising potential of repurposing type 2 diabetes (T2D) medications for treatment Parkinson's disease (PD), highlighting shared pathophysiological mechanisms between these two age-related conditions, such as oxidative stress, mitochondrial dysfunction, and ferroptosis. The overlap suggests that existing drugs could target common pathways involved in both conditions. Specifically, discusses how T2D medications, including metformin (Met), peroxisome-proliferator-activated receptor gamma (PPAR-γ) agonists, sodium-glucose cotransporter-2 (SGLT2) inhibitors, incretins, dipeptidyl-peptidase 4 (DPP-4) can improve function, reduce neuroinflammation potentially inhibit connection ferroptosis treatments, medication, are only beginning to be explored. limited data attributed also complexity fact specific role pathogenesis has not been a primary focus until recent. Despite preclinical evidence, clinical findings mixed, underscoring need further research elucidate drugs' roles neurodegeneration. Repurposing have well-established safety profiles significantly time cost associated with drug development offer more comprehensive approach managing compared treatments targeting single mechanism.

Language: Английский

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The Impact of Chronic Diseases on Cognitive Impairment in Rural Population of India: A Focus on Diabetes, Hypertension, Cardiovascular Disease, and Stroke

Brain Behavior and Immunity Integrative, Journal Year: 2025, Volume and Issue: unknown, P. 100107 - 100107

Published: Feb. 1, 2025

Language: Английский

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Development of hyaluronic acid-based hydrogels for chronic diabetic wound healing: A review

International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: unknown, P. 142273 - 142273

Published: March 1, 2025

Language: Английский

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The Role of Hypothalamic Microglia in the Onset of Insulin Resistance and Type 2 Diabetes: A Neuro-Immune Perspective

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(23), P. 13169 - 13169

Published: Dec. 7, 2024

Historically, microglial activation has been associated with diseases of a neurodegenerative and neuroinflammatory nature. Some, like Alzheimer's disease, Parkinson's multiple system atrophy, have explored extensively, while others pertaining to metabolism not so much. However, emerging evidence points hypothalamic inflammation mediated by microglia as driver metabolic dysregulations, particularly insulin resistance type 2 diabetes mellitus. Here, we explore this connection further examine pathways that underlie relationship, including the IKKβ/NF-κβ, IRS-1/PI3K/Akt, mTOR-S6 Kinase, JAK/STAT, PPAR-γ signaling pathways. We also investigate role non-coding RNAs, namely microRNAs long in related neuroinflammation their diagnostic therapeutic potential. Finally, therapeutics further, searching for both pharmacological non-pharmacological interventions can help mitigate activation.

Language: Английский

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Pathology and Treatments of Alzheimer’s Disease Based on Considering Changes in Brain Energy Metabolism Due to Type 2 Diabetes

Molecules, Journal Year: 2024, Volume and Issue: 29(24), P. 5936 - 5936

Published: Dec. 16, 2024

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder with cognitive dysfunction, memory decline, and behavioral disturbance, it pathologically characterized by the accumulation of amyloid plaques neurofibrillary tangles in brain. Although various hypotheses have been proposed to explain pathogenesis AD, including beta hypothesis, oxidative stress abnormal phosphorylation tau proteins, exact pathogenic mechanisms underlying AD remain largely undefined. Furthermore, effective curative treatments are very limited. Epidemiologic studies provide convincing evidence for significant association between type 2 diabetes AD. Here, we showed energy metabolism using glucose, lactate, ketone bodies, lipids as substrates normal brain, changes such due diabetes. We also influences altered on pathology comprehensively searched risk factors related possible therapeutic interventions based considering brain development

Language: Английский

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