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The prognostic impact of arterial spin labeling hyperperfusion in acute ischemic stroke: a systematic review and meta-analysis.
Acta Radiol
January 2025
Department of Radiology & Institute of Rehabilitation and Development of Brain Function, Nanchong Central Hospital, The Second Clinical Medical College of North Sichuan Medical College, Nanchong, Sichuan, PR China.
Hyperperfusion is related to vessel recanalization, tissue reperfusion, and collateral circulation. To determine the prognostic impact of hyperperfusion after an acute ischemic stroke (AIS) identified by arterial spin labeling (ASL) cerebral blood flow. Studies published in PubMed, Embase, and Cochrane Library databases were searched.
View Article and Find Full Text PDFIntranasal iron administration induces iron deposition, immunoactivation, and cell-specific vulnerability in the olfactory bulb of C57BL/6 mice.
Zool Res
January 2025
School of Basic Medicine, Institute of Brain Science and Disease, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Brain Diseases, Qingdao University, Qingdao, Shandong, 266071, China. E-mail:
Iron is the most abundant transition metal in the brain and is essential for brain development and neuronal function; however, its abnormal accumulation is also implicated in various neurological disorders. The olfactory bulb (OB), an early target in neurodegenerative diseases, acts as a gateway for environmental toxins and contains diverse neuronal populations with distinct roles. This study explored the cell-specific vulnerability to iron in the OB using a mouse model of intranasal administration of ferric ammonium citrate (FAC).
View Article and Find Full Text PDFDNA2 knockout aggravates cerebral ischemia/reperfusion injury by reducing postsynaptic Homer1a.
Zool Res
January 2025
Research & Development Institute of Northwestern Polytechnical University in Shenzhen, Shenzhen, Guangdong 518057, China.
DNA2, a multifunctional enzyme with structure-specific nuclease, 5 -to-3 helicase, and DNA-dependent ATPase activities, plays a pivotal role in the cellular response to DNA damage. However, its involvement in cerebral ischemia/reperfusion (I/R) injury remains to be elucidated. This study investigated the involvement of DNA2 in cerebral I/R injury using conditional knockout (cKO) mice ( -Cre) subjected to middle cerebral artery occlusion (MCAO), an established model of cerebral I/R.
View Article and Find Full Text PDFMolecular profiling of frontal and occipital subcortical white matter hyperintensities in Alzheimer's disease.
Front Neurol
January 2025
Department of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
White matter hyperintensities (WMHs) are commonly detected on T2-weighted magnetic resonance imaging (MRI) scans, occurring in both typical aging and Alzheimer's disease (AD). Despite their frequent appearance and their association with cognitive decline in AD, the molecular factors contributing to WMHs remain unclear. In this study, we investigated the transcriptomic profiles of two commonly affected brain regions with coincident AD pathology-frontal subcortical white matter (frontal-WM) and occipital subcortical white matter (occipital-WM)-and compared with age-matched cognitively intact controls.
View Article and Find Full Text PDFBrain microstructure alterations in subjective cognitive decline: a multi-component T2 relaxometry study.
Brain Commun
January 2025
Department of Clinical Psychology and Psychobiology, Universidade de Santiago de Compostela (USC), Santiago de Compostela 15782, Spain.
Previous research has revealed patterns of brain atrophy in subjective cognitive decline, a potential preclinical stage of Alzheimer's disease. However, the involvement of myelin content and microstructural alterations in subjective cognitive decline has not previously been investigated. This study included three groups of participants recruited from the Compostela Aging Study project: 53 cognitively unimpaired adults, 16 individuals with subjective cognitive decline and hippocampal atrophy and 70 with subjective cognitive decline and no hippocampal atrophy.
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