Background: Vascular risk factors, including inflammation, may contribute to dementia development. We investigated the associations between peripheral inflammatory biomarkers and cognitive decline in five domains (memory, construction, language, psychomotor speed, and executive function).
Methods: Community-dwelling older adults from the Ginkgo Evaluation of Memory Study (n = 1,159, aged 75 or older) free of dementia at baseline were included and followed for up to 7 years. Ten biomarkers were measured at baseline representing different sources of inflammation: vascular inflammation (pentraxin 3 and serum amyloid P), endothelial function (endothelin-1), metabolic function (adiponectin, resistin, and plasminogen activating inhibitor-1), oxidative stress (receptor for advanced glycation end products), and general inflammation (interleukin-6, interleukin-2, and interleukin-10). A combined z-score was created from these biomarkers to represent total inflammation across these sources. We utilized generalized estimating equations that included an interaction term between z-scores and time to assess effect of inflammation on cognitive decline, adjusting for demographics (such as age, race/ethnicity, and sex), cardiovascular risk factors, and apolipoprotein E ε4 carrier status. A Bonferroni-adjusted significance level of .01 was used. We explored associations between individual biomarkers and cognitive decline without adjustment for multiplicity.
Results: The combined inflammation z-score was significantly associated with memory and psychomotor speed (p < .01). Pentraxin 3, serum amyloid P, endothelin-1, and interleukin-2 were associated with change in at least one cognitive domain (p < .05).
Conclusion: Our results suggest that total inflammation is associated with memory and psychomotor speed. In particular, systemic inflammation, vascular inflammation, and altered endothelial function may play roles in domain-specific cognitive decline of nondemented individuals.
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http://dx.doi.org/10.1093/gerona/glw155 | DOI Listing |
ACS Chem Neurosci
January 2025
Department of Bioengineering and Biotechnology, Birla Institute of Technology Mesra, Ranchi, Jharkhand 835215, India.
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National Key Laboratory of Human Factors Engineering, China Astronaut Research and Training Centre, Beijing, China.
Objective: Attention forms the foundation for the formation of situation awareness. Low situation awareness can lead to driving performance decline, which can be dangerous in driving. The goal of this study is to investigate how different types of pre-takeover tasks, involving cognitive, visual and physical resources engagement, as well as individual attentional function, affect driver's attention restoration in conditionally automated driving.
View Article and Find Full Text PDFMedicine (Baltimore)
January 2025
Department of Anesthesiology, Affiliated Hospital of Southwest Jiaotong University, The Third People's Hospital of Chengdu, Chengdu, China.
Background: This study compares the outcomes of general anesthesia (GA) and regional anesthesia (RA) in geriatric hip fracture surgery to determine optimal anesthesia strategies for this population.
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Exp Physiol
January 2025
Department of Physiology, School of Medicine, University College Cork, Cork, Ireland.
Absence of the structural protein, dystrophin, results in the neuromuscular disorder Duchenne Muscular Dystrophy (DMD). In addition to progressive skeletal muscle dysfunction, this multisystemic disorder can also result in cognitive deficits and behavioural changes that are likely to be consequences of dystrophin loss from central neurons and astrocytes. Dystrophin-deficient mdx mice exhibit decreases in grey matter volume in the hippocampus, the brain region that encodes and consolidates memories, and this is exacerbated with ageing.
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January 2025
Faculty of Medicine, "Transilvania" University, Brasov, Romania; and.
Background: Dementia leads to cognitive decline affecting memory, thinking, and behavior. Current pharmaceutical treatments are symptomatic, with limited efficacy and significant drawbacks. Ginkgo biloba extract (EGb761) is being explored as an adjuvant therapy for dementia because of its potential neuroprotective effects.
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