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neurovascular
229 studies tagged neurovascular, dated 1986-03-01 to 2026-10-24. Bibliography: BibTeX (.bib) · RIS (.ris)
Newest in this topic
- Serpin A3 is Increased in Cerebral Amyloid Angiopathy and ARIA 2026-10-24
- Endothelial CD36 links arteriolar remodeling to metabolic and immune alterations in Alzheimer’s disease 2026-10-14
- Location-specific Longitudinal Patterns of Subcortical and Lobar Cerebral Microhemorrhages in Preclinical Alzheimer Disease 2026-10-13
Studies
229 studies carry this tag.
Date range
1986 to 2026
Top journals
- Journal of Alzheimer's disease : JAD 13
- International journal of molecular sciences 11
- bioRxiv 11
- Alzheimer's & dementia : the journal of the Alzheimer's Association 10
- Molecular neurodegeneration 7
123 journals in all.
Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.
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Vascular pathology is an important contributor to dementia, and astrocyte dysfunction is increasingly recognized as a key mediator of cerebrovascular injury.
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Alzheimer’s disease (AD) is accompanied by profound cerebrovascular dysfunction, yet it remains unclear whether endothelial abnormalities reflect only vascular injury or altered regulatory states connecting vascular remodeling with metabolic and immune function.
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Emerging evidence and expert opinion suggest that subcortical microhaemorrhages may be less closely related to cerebral amyloidosis than lobar lesions and may therefore warrant separate consideration in anti-amyloid treatment eligibility criteria.
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Vascular dementia (VaD) is a prevalent and devastating neurocognitive disorder characterized by profound white matter damage, yet the precise cellular mechanisms linking cerebrovascular stress to demyelination remain poorly understood.
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Blood-brain barrier (BBB) malfunction contributes to pathophysiology of Alzheimer’s disease (AD), yet the mechanisms that confer hippocampal endotheliocytes vulnerability remain unclear.
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Cerebrospinal fluid (CSF) flow and the glymphatic system are essential for maintaining brain homeostasis, yet the precise mechanisms driving their profound failure in Alzheimer’s disease (AD) remain largely elusive.
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Variants at the CD2AP locus, which encodes a branched-actin regulator, are associated with late-onset Alzheimer’s disease (AD), and CD2AP-deficient mice show increased blood-brain barrier (BBB) permeability.
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Accumulation of proteins such as amyloid β (Aβ), hyperphosphorylated tau and α-synuclein within the brain alters neural information processing and causes neurodegeneration 1–3 , but how toxic solutes are cleared from the brain remains highly controversial 4,5 .
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16/100
Elevated terminal sialylation of neutrophil glycoproteins contributes to capillary stalling and cerebral hypoperfusion in AD.
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White matter hyperintensities (WMHs) are a hallmark of cerebral small vessel disease, commonly seen in cognitively normal older adults and patients with neurodegenerative disorders, and are thought to reflect varying degrees of tissue damage.
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Cerebrospinal fluid (CSF) flows through perivascular spaces (PVSs) surrounding brain vasculature, and impaired flow has been linked to neurodegenerative diseases such as Alzheimer’s. However, the mechanisms driving CSF flow and its oscillatory dynamics remain poorly understood.
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Traumatic brain injury (TBI) is the main cause of death and disability in the United States in people younger than 35 years old and is a common cause of wartime injuries.
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A major obstacle to effective Alzheimer’s disease therapy is the limited ability to deliver therapeutics across the blood-brain barrier.
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The brain endothelial Gαq/11 signalling pathway preserves normal vascular reactivity, and its loss resembles mild endothelial dysfunction in the brain.
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63/100
In multivariable analyses, none of the plasma biomarkers were significantly associated with cognitive impairment.
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Monoclonal antibodies targeting amyloid-β are the first approved disease-modifying treatment for Alzheimer’s disease.
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Anti-amyloid antibody treatment for Alzheimer’s disease is linked to Amyloid-Related Imaging Abnormalities (ARIA), including vasogenic edema (ARIA-E) and microhemorrhages (ARIA-H), especially in ApoE ε4/4 carriers.
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Anti-Aβ immunotherapies for Alzheimer’s Disease (AD) have high rates of amyloid-related imaging abnormalities (ARIA), an adverse side effect with markedly higher rates in APOE4 carriers.
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An age-related decline in vasodilation mediated by neurovascular nitric oxide (NO) and vasoconstriction driven by the Piezo1 receptor precede the aggregation of soluble brain proteins such as amyloid-β (Aβ), which then causes further disruption of brain solute homeostasis, ultimately leading to neurodegeneration in Alzheimer’s disease.
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The etiology of cerebrovascular pathology is heterogeneous.
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CAA-PRS was significantly associated with pathological CAA (OR = 1.766, p < 0.001), with an AUC of 0.783 overall and 0.766 (OR = 1.780, p = 0.002) in those with high amyloid burden.
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Alzheimer's disease (AD) is widely recognized as a multifactorial disorder involving neurovascular and glial dysfunction beyond amyloid-β and tau pathology.
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48/100
Cerebral amyloid angiopathy (CAA) is a small vessel disease characterized by the deposition of amyloid-beta in small cerebral vessels, which can lead to intracerebral hemorrhages and cognitive impairment.
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16/100
Cerebral small vessel disease (CSVD) is strongly linked to metabolic risk factors and represents a major cause of vascular cognitive impairment and dementia.
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The blood-brain barrier (BBB) is a critical structure for maintaining homeostasis in the central nervous system, and its dysfunction is widely implicated in the pathogenesis and progression of various neurological disorders.
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Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder characterized by the accumulation of amyloid-beta (Aβ) in the walls of cerebral vessels.
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Cerebral small vessel disease (cSVD) is the most common cause of vascular cognitive impairment and dementia (VCID) and highly associated with Alzheimer's disease pathogenesis.
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AD mice showed early decreases in NVC and bilateral connectivity (BC) in motor and cingulate cortex, and hypoconnectivity within the sensory-motor network.
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FUS-enhanced delivery of AAV resulted in a 12.6% knockdown of APOE ε4 gene expression in the targeted hippocampus, accompanied by an over 20% decrease in apoE4 protein levels and significant reductions in astrocyte and microglia levels.
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45/100
The prevalence of cerebral amyloid angiopathy (CAA) has been shown to increase with age, with rates reported to be around 50-60% in individuals over 80 years old who have cognitive impairment.
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Amyloid-related imaging abnormalities (ARIA) are parenchymal edema/effusion and hemorrhage that occur as side effects of immunotherapies targeting beta-amyloid for patients with Alzheimer's disease (AD).
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With our focus on Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), the authors herein provided a comprehensive overview of impaired amyloid beta and tau clearance pathways observed through advanced neuroimaging techniques such as dynamic contrast-enhanced MR imaging, arterial spin labeling, phase contrast MR imaging, PET, and functional MR imaging.
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Ischemic stroke and vascular cognitive impairment, caused by a sudden arterial occlusion or more subtle but protracted vascular insufficiency, respectively, are leading causes of morbidity and mortality worldwide with limited therapeutic options.
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Cerebral small vessel disease (SVD) is a vascular disorder that increases the risk of stroke and dementia and is diagnosed through brain MRI.
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Chronic neuroinflammation is a principal cause of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
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Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease characterized by vascular amyloid-β (Aβ) deposition.
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β-blockers that easily cross the blood-brain barrier (BBB) seem to diminish the risk of Alzheimer's disease (AD), hypothetically facilitating waste clearance.
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Neurovascular unit (NVU) inflammation via activation of glial cells and neuronal damage plays a critical role in neurodegenerative diseases.
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Our study has established a significant link between CAA-Aβ antibody immune complex formation, immune activation and vascular damage leading to smooth muscle cell loss.
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Worldwide, around 50 million people live with dementia, and this number is projected to triple by 2050.
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Cerebral small vessel disease (CSVD) is a group of pathologies that affect the cerebral blood vessels.
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As shown previously, there was a robust association between Lin bodies and GFAP-positive astrocyte processes.
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A total of 124 participants with Alzheimer disease, cerebrovascular disease, or a mix Alzheimer's and cerebrovascular diseases and 55 controlparticipants underwent magnetic resonance imaging and neuropsychological testing.
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Forty-four participants were recruited between September 2019 and June 2022.
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55/100
Cerebrovascular reactivity (CVR) deficits may contribute to small vessel disease, such as white matter hyperintensities (WMH).
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The glymphatic movement of fluid through the brain removes metabolic waste 1-4 .
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Age-associated cerebral small vessel disease (CSVD) represents a clinically heterogenous condition, arising from diverse microvascular mechanisms.
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Cerebral small vessel disease and glymphatic dysfunction are anatomically connected and significant risk factors are shared between the two.
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The brain vascular system receives one-fifth of the total oxygen from the cardiac output, and this transport system is highly dependent on blood-brain barrier (BBB) integrity.
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These results indicate a strong association between WMH and MCH, a common manifestation of cerebral amyloid angiopathy and ARIA-H. These results suggest that increased WMH volume may represent an early sign of vessel amyloidosis, likely prior to the emergence of MCH.
From across this tag
7 of the 229 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 7. The same 7 appear here every time.
- Border-associated macrophages promote cerebral amyloid angiopathy and cognitive impairment through vascular oxidative stress
- Experimental Rodent Models of Vascular Dementia: A Systematic Review
- Cerebral Small Vessel Disease: A Review Focusing on Pathophysiology, Biomarkers, and Machine Learning Strategies
- Real-time whole-brain imaging of hemodynamics and oxygenation at micro-vessel resolution with ultrafast wide-field photoacoustic microscopy
- Blood-Brain Barrier Leakage in Patients with Early Alzheimer Disease
- Neurovascular coupling in the normal brain and in hypertension, stroke, and Alzheimer disease
- Cerebral amyloid angiopathy with focal presentation-about 3 cases