Purpose: To assess the prevalence and number of cortical microinfarcts in patients with Alzheimer disease (AD) by using a 7-T magnetic resonance (MR) imaging system, to assess the independent association of cortical microinfarcts with cognitive dysfunction, and to investigate potential confounding effects of the coexisting presence of cerebral amyloid angiopathy (CAA).
Materials And Methods: The local institutional review board approved this study. In all cases, informed consent was obtained. High-spatial-resolution fluid-attenuated inversion recovery and T2*-weighted images were acquired in 14 AD patients and 18 control subjects to assess the presence of microinfarcts and microbleeds. Presence of CAA was assessed according to the Boston criteria. Image analysis was performed independently by two reviewers. Mann-Whitney U test was performed to assess differences in number of microinfarcts between groups. Negative binomial regression models were used to assess the association between diagnosis of AD and diagnosis of CAA and number of microinfarcts, between diagnosis of AD and number of microbleeds and number of microinfarcts, and between cognitive function and number of microinfarcts, all corrected for age and sex.
Results: Interobserver agreement was excellent for detecting microinfarcts (κ = 0.91) (P < .001). Patients with AD demonstrated higher number (P = .005) of microinfarcts (mean, 7.2) compared with control subjects (mean, 1.8). Negative binomial regression models showed an independent association between AD and number of microinfarcts (P = .006) and a trend for CAA and microinfarcts (P = .052). A negative correlation was found between cognitive function and the number of microinfarcts (P = .009).
Conclusion: Patients with AD show more microinfarcts than do control subjects, the number of microinfarcts correlates with global cognitive performance, and the presence of microinfarcts was mainly AD rather than CAA related.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1148/radiol.13130743 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL, USA.
Background: Hemoglobin A1C (A1C) is a measure of long-term glycemic control. In a previous study using a single measure of A1C, we showed that it is related to postmortem cerebrovascular pathology. Here, we use annually collected A1C data to study the relationship of A1C average and variability over time with neuropathology in a large number of older adults with and without diabetes.
View Article and Find Full Text PDFClinical Manifestations.
Alzheimers Dement
December 2024
Banner Sun Health Research Institute, Phoenix, AZ, USA.
Background: Mild Cognitive Impairment (MCI) is a pre-dementia state where impaired cognitive domains (memory, executive, visuospatial processing, language) may predict underlying pathology, e.g. Alzheimer's disease(AD), Lewy body (LB), and other.
View Article and Find Full Text PDFExpression of alpha smooth muscle actin decreases with ageing and increases upon lumen obstruction in mouse brain pericytes.
Geroscience
November 2024
Institute of Biophysics, HUN-REN Biological Research Centre, Szeged, Hungary.
Cerebral pericytes are mural cells covering brain microvessels, organized as ensheathing, mesh and thin-strand pericytes. These latter two, together called capillary pericytes, have low levels of alpha smooth muscle actin (α-SMA), regulating basal vascular tone and applying a slow influence on cerebral blood flow. Pericytes are subject to alterations in ageing which may be even more pronounced in age-related pathologies, including microinfarcts, which usually affect a large number of vessels in the ageing brain.
View Article and Find Full Text PDFPathologic and clinical correlates of region-specific brain GFAP in Alzheimer's disease.
Acta Neuropathol
November 2024
Vanderbilt Memory and Alzheimer's Center, Vanderbilt University Medical Center, Nashville, TN, USA.
Plasma glial fibrillary acidic protein (GFAP) is an emerging biomarker of Alzheimer's disease (AD), with higher blood GFAP levels linked to faster cognitive decline, particularly among individuals with high brain amyloid burden. However, few studies have examined brain GFAP expression to clarify if peripheral associations reflect brain changes. This study aimed to correlate region-specific GFAP mRNA expression (n = 917) and protein abundance (n=386) with diverse neuropathological measures at autopsy in the Religious Orders Study and Rush Memory and Aging Project (ROS/MAP) and to characterize the interaction between brain GFAP and brain amyloid burden on downstream outcomes.
View Article and Find Full Text PDFContinuous theta burst stimulation ameliorates cognitive deficits in microinfarcts mice via inhibiting glial activation and promoting paravascular CSF-ISF exchange.
Neuroscience
November 2024
Department of Geriatric Neurology, Guangxi Academy of Medical Sciences & the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, China. Electronic address:
Article Synopsis
- * The study assessed cTBS effects on mice with microinfarcts by measuring spatial learning via the Morris water maze and using advanced imaging techniques to evaluate brain changes.
- * Results indicated that cTBS improved memory, enhanced brain clearance mechanisms, increased neuron survival, and reduced harmful glial cell activation, showcasing its potential to protect against cognitive dysfunction in microinfarcts.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!