Background: Diabetes mellitus (DM) is known to be a risk factor for dementia. However, it is unclear if hypoglycemic events play a role in the risk of dementia. We aimed to systematically review evidence on the risk of dementia in DM patients based on prior hypoglycemic events.
Methods: PubMed, Embase, ScienceDirect, CENTRAL, and Google Scholar databases were searched till 15th November 2021 for cohort studies assessing the risk of dementia based on prior hypoglycemic events in DM patients. Adjusted data were pooled in a random-effects model.
Results: Ten studies with a total of 1,407,643 patients were included. Pooled analysis of all ten studies indicated that hypoglycemic episodes were associated with a statistically significant increase in the risk of dementia in DM patients as compared to those not experiencing hypoglycemic episodes (HR: 1.44 95% CI: 1.26, 1.65 I= 89% p < 0.00001). The results did not change on the exclusion of any study. Sub-group analysis based on the study population, type of study, adjustment for glycated hemoglobin, gender, and the number of hypoglycemic episodes also presented similar results.
Conclusions: Evidence from observational studies with a large sample size indicates that DM patients with hypoglycemic episodes are at increased risk of dementia. Anti-hyperglycemic drugs should be adequately tailored in these patients to avoid the risk of dementia.
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http://dx.doi.org/10.1186/s13098-022-00799-9 | DOI Listing |
J Gen Intern Med
January 2025
Northwell Health, New Hyde Park, NY, USA.
Background: Oropharyngeal dysphagia (dysphagia) is a common (up to 86%) and devastating syndrome in hospitalized older adults with dementia.
Objective: To describe the perspectives of dysphagia management in hospitalized patients with dementia among hospital medicine providers (i.e.
Commun Biol
January 2025
School of Psychology and Sussex Neuroscience, University of Sussex, Brighton, UK.
Reduced cerebral blood flow occurs early in the development of Alzheimer's disease (AD), but the factors producing this reduction are unknown. Here, we ask whether genetic and lifestyle risk factors for AD-the ε4 allele of the Apolipoprotein (APOE) gene, and physical activity-can together produce this reduction in cerebral blood flow which leads eventually to AD. Using in vivo two-photon microscopy and haemodynamic measures, we record neurovascular function from the visual cortex of physically active or sedentary mice expressing APOE3 and APOE4 in place of murine APOE.
View Article and Find Full Text PDFMol Psychiatry
January 2025
Department of Psychological Medicine and Clinical Neuroscience, Cardiff University, United Kingdom and UK Dementia Research Institute at Cardiff, Cardiff University, Cardiff, UK.
In this perspective we draw together the data from the genome wide association studies for Alzheimer's disease, Parkinson's disease and the tauopathies and reach the conclusion that in each case, most of the risk loci are involved in the clearance of the deposited proteins: in Alzheimer's disease, the microglial removal of Aβ, in the synucleinopathies, the lysosomal clearance of synuclein and in the tauopathies, the removal of tau protein by the ubiquitin proteasome. We make the point that most loci identified through genome wide association studies are not strictly pathogenic but rather relate to failures to remove age related damage. We discuss these issues in the context of copathologies in elderly individuals and the prediction of disease through polygenic risk score analysis at different ages.
View Article and Find Full Text PDFThorax
January 2025
Center for Sleep and Vigilance Disorders, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Exp Gerontol
January 2025
Department of Clinical Sciences and Community Health, University of Milan, Via della Commenda 19, 20122 Milan, Italy; Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico, Via Francesco Sforza 35, 20122 Milan, Italy. Electronic address:
Background: During aging, there is a progressive impairment of immune cell function that triggers the production of pro-inflammatory cytokines causing the so-called "inflammaging". Frailty represents a condition of increased vulnerability to stresses and reduced homeostatic reserve reflecting not only health status but also biological age. In older subjects without dementia, we showed that markers of inflammaging were differently associated with chronological age than with frailty.
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