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Microinfarcts are widespread in the elderly, accompanied by varying degrees of cognitive decline. Continuous theta burst stimulation (cTBS) has been demonstrated to be neuroprotective on cognitive dysfunction, but the underlying cellular mechanism has been still not clear. In the present study, we evaluated the effects of cTBS on cognitive function and brain pathological changes in mice model of microinfarcts. The spatial learning and memory was assessed by Morris water maze (MWM), Glymphatic clearance efficiency was evaluated using in vivo two-photon imaging. The loss of neurons, activation of astrocytes and microglia, the expression and polarity distribution of the astrocytic aquaporin-4 (AQP4) were assessed by immunofluorescence staining. Our results showed that cTBS treatment significantly improved the spatial learning and memory, accelerated the efficiency of glymphatic clearance, up-regulated the AQP4 expression and improved the polarity distribution of AQP4 in microinfarcts mice. Besides, cTBS treatment increased the number of surviving neurons, whereas decreased the activated astrocytes and microglia. Our study suggested that cTBS accelerated glymphatic clearance and inhibited the excessive gliogenesis, which ultimately exerted neuroprotective effects on microinfarcts mice.
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http://dx.doi.org/10.1016/j.neuroscience.2024.09.046 | DOI Listing |
Adv Sci (Weinh)
June 2025
Department of Electrical and Computer Engineering, Rice University, Houston, TX, 77005, USA.
Microinfarcts, the "invisible lesions", are prevalent in aged and injured brains and associated with cognitive impairments, yet their neurophysiological impact remains largely unknown. Using a multimodal chronic neural platform that combines functional microvasculature imaging with spatially resolved neural recording, the neurovascular effect of a single microinfarct is investigated. Unlike larger strokes, microinfarcts induced only temporary suppression of neural activity with minimal cell death, with recovery paralleling vasculature remodeling at the infarct core.
View Article and Find Full Text PDFJ Vis Exp
November 2024
Department of Neurology, University of Pittsburgh; Geriatric Research Education and Clinical Center, VA Pittsburgh Healthcare System;
Vascular cognitive impairment and dementia (VCID) results from vascular brain injury. Given VCID's high incidence, which is expected to continue rising as the population ages, it is critical to establish a robust animal model for the disease. This paper presents a novel method of creating a mouse model of VCID that is based on asymmetric bilateral common carotid artery stenosis, which mimics human chronic cerebral hypoperfusion caused by carotid atherosclerosis.
View Article and Find Full Text PDFAdv Mater
January 2025
Beijing Advanced Innovation Center for Soft Matter Science and Engineering, College of Life Science and Technology, College of Materials Science and Engineering, Beijing University of Chemical Technology, Beijing, 100029, China.
Geroscience
April 2025
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 PDFNeuroscience
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: