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Differences between private and public primary health care centers and differences between men and women in antihypertensive care and cardiovascular prevention in all patients with hypertension treated in primary care in Stockholm County, Sweden.
BMC Prim Care
January 2025
Division of Family Medicine and Primary Care, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Huddinge, Sweden.
Aims: To study differences in cardiovascular prevention and hypertension management in primary care in men and women, with comparisons between public and privately operated primary health care (PHC).
Methods: We used register data from Region Stockholm on collected prescribed medication and registered diagnoses, to identify patients aged 30 years and above with hypertension. Age-adjusted logistic regression was used to calculate odds ratios (ORs) with 99% confidence intervals (99% CIs) using public PHC centers as referents.
Evaluating amyloid-beta aggregation and toxicity in transgenic Caenorhabditis elegans models of Alzheimer's disease.
Methods Cell Biol
January 2025
Federal University of Santa Maria, Center for Natural and Exact Sciences, Department of Biochemistry and Molecular Biology, Graduate Program in Biological Sciences: Toxicological Biochemistry, Camobi, Santa Maria, RS, Brazil.
Alzheimer's disease (AD) is the leading cause of dementia in the elderly, clinically characterized by memory loss, cognitive decline, and behavioral disturbances. Its pathogenesis is not fully comprehended but involves intracellular depositions of amyloid beta peptide (Aβ) and neurofibrillary tangles of hyperphosphorylated tau. Currently, pharmacological interventions solely slow the progression of symptoms.
View Article and Find Full Text PDFThe current models unravel the molecular mechanisms underlying the intricate pathophysiology of Alzheimer's disease using zebrafish.
Methods Cell Biol
January 2025
Department of Pharmacology, SPP School of Pharmacy & Technology Management, Mumbai, India. Electronic address:
The foremost cause of dementia is Alzheimer's disease (AD). The vital pathological hallmarks of AD are amyloid beta (Aβ) peptide and hyperphosphorylated tau (p-tau) protein. The current animal models used in AD research do not precisely replicate disease pathophysiology, making it difficult for researchers to quickly and effectively gather data or screen potential therapy possibilities.
View Article and Find Full Text PDFEvaluating polyglutamine protein aggregation and toxicity in transgenic Caenorhabditis elegans models of Huntington's disease.
Methods Cell Biol
January 2025
State University of Minas Gerais, Department of Biomedical Sciences and Health, Passos, MG, Brazil. Electronic address:
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by a repeat of the cytosine-adenine-guanine trinucleotide (CAG) in the huntingtin gene (HTT). This results in the translation of a mutant huntingtin (mHTT) protein with an abnormally long polyglutamine (polyQ) repeat. The pathology of HD leads to neuronal cell loss, motor abnormalities, and dementia.
View Article and Find Full Text PDFAssociation of statins use and genetic susceptibility with incidence of Alzheimer's disease.
J Prev Alzheimers Dis
February 2025
Department of Neurology, Fujian Medical University Union Hospital, Fujian Key Laboratory of Molecular Neurology and Institute of Neuroscience, Fujian Medical University, No.29, Xinquan Road, Gulou District, Fuzhou, Fujian Province, 350000, China; Institute of Clinical Neurology, Fujian Medical University, No.29 Xinquan Road, Gulou District, Fuzhou, Fujian Province, 350000, China. Electronic address:
Background: The effect of statins use on the incidence of Alzheimer's disease (AD) is still under debate, and it could be modified by a series of factors.
Objectives: We aimed to examine the association of statins use with the risk of cognitive impairment and AD, and assess the moderating roles of genetic susceptibility and other individual-related factors.
Design: A longitudinal study was conducted from the UK Biobank where individuals completed baseline surveys (2006-2010) and were followed (mean follow-up period: 9 years).
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