Background: Recent studies have suggested that atherosclerosis contributes to the development of dementia of the Alzheimer's type (DAT). Convenient and valid biochemical markers of DAT are needed to control risk factors for this disease. The aims of the present study were thus (1) to determine the distribution of plasma beta-amyloid peptide1-42 (Abeta1-42) levels in an older population and (2) to investigate factors correlating with plasma levels of this amyloid peptide. Our data support the hypothesis that atherosclerosis plays a role in the pathogenesis of DAT.
Methods: 759 Japanese community residents participated in a municipal medical health evaluation; a subset of 280 was selected at random for the measurement of physiological, psychosocial and life-style variables, together with the analysis of blood specimens for cell counts, hematocrit, Abeta1-42, and other biochemical markers.
Results: Log-transformed plasma Abeta1-42 concentrations showed a Gaussian distribution. Quartiles of log10 (Abeta1-42) concentrations correlated significantly with age categories, but not with other sociopsychological and life-style variables. Plasma Abeta1-42 was significantly correlated with systolic and diastolic blood pressure (DBP; r = 0.19, p = 0.002 and r = 0.16, p = 0.007, respectively), pulse pressure (r = 0.13, p = 0.036), total cholesterol (r = 0.15, p = 0.011), log10 (triacyl glycerol) (r = 0.14, p = 0.021), and log10 (hemoglobin A1c) [log10 (HbA1c)] (r = 0.14, p = 0.020). Stepwise multiple regression analysis showed significant independent effects of DBP, and log(10) (HbA1c) on plasma Abeta1-42 concentrations.
Conclusions: Our findings suggest that conventional atherosclerotic risk factors are associated with plasma Abeta1-42 levels. This observation may be important in the detection and prevention of DAT.
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http://dx.doi.org/10.1159/000073765 | DOI Listing |
Introduction: Previous studies have examined the predictive accuracy of plasma amyloid beta (Aβ) biomarkers in clinical cohorts. However, their accuracy for predicting amyloid-positive patients in community-based cohorts is unclear. This study aimed to determine the predictive accuracy of Aβ precursor protein 669-711/Aβ1-42, Aβ1-40/1-42 and their composite biomarkers for brain amyloid deposition or the clinical progression in community-dwelling older adults with mild cognitive impairment (MCI).
View Article and Find Full Text PDFSci Rep
November 2024
Institute of Preclinical Sciences, Veterinary Faculty, University of Ljubljana, Gerbičeva 60, Ljubljana, 1000, Slovenia.
Dementia, especially Alzheimer's disease, presents a major clinical challenge, and researchers are still searching for an optimal animal model. To address this gap, we compared male and ovariectomized female C57BL/6 mice treated with 30 mg/kg aftin-4, which induces neurodegeneration, with naturally aged (15-16 months old) mice not treated with aftin-4. We performed a series of behavioral tests; measured postmortem plasma β-amyloid levels (Aβ1-40 and Aβ1-42) and the levels of the oxidative stress indicators glutathione peroxidase (GPx), superoxide dismutase (SOD) and malondialdehyde (MDA); and evaluated astrocytic reactivity in the brain using glial fibrillary acid protein (GFAP) levels.
View Article and Find Full Text PDFAlzheimers Res Ther
September 2024
Department NVS, Division of Neurogeriatrics, Center for Alzheimer Research, Karolinska Institutet, Visionsgatan 4, Bioclinicum, Solna, J10:20, 171 64, Sweden.
Background: Several blood-based biomarkers offer the opportunity of in vivo detection of brain pathology and neurodegeneration in Alzheimer disease with high specificity and sensitivity, but the performance of amyloid-β (Aβ) measurements remains under evaluation. Autosomal dominant Alzheimer disease (ADAD) with mutations in PSEN1, PSEN2 and APP can be studied as a model for sporadic Alzheimer disease. However, clarifying the genetic effects on the Aβ-levels in different matrices such as cerebrospinal fluid or plasma is crucial for generalizability and utility of data.
View Article and Find Full Text PDFFluids Barriers CNS
September 2024
Department of Neurology, Tianjin Dementia Institute, Tianjin Key Laboratory of Cerebrovascular and Neurodegenerative Diseases, Tianjin Huanhu Hospital, 6 Jizhao Road, Jinnan District, Tianjin, 300350, People's Republic of China.
High-performance, resource-efficient methods for plasma amyloid-β (Aβ) quantification in Alzheimer's disease are lacking; existing mass spectrometry-based assays are resource- and time-intensive. We developed a streamlined mass spectrometry method with a single immunoprecipitation step, an optimized buffer system, and ≤75% less antibody requirement. Analytical and clinical performances were compared with an in-house reproduced version of a well-known two-step assay.
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