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blood-brain-barrier
229 studies tagged blood-brain-barrier, 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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In recent years, studies have demonstrated that hypertension-related changes (e.g., small vascular lesions, inflammatory reactions, hypoperfusion, oxidative stress, damage to autoregulatory processes and the blood-brain barrier, and cerebral amyloid angiopathy) can occur over time in cerebral small vessels, potentially leading to lower cognitive function when blood pressure (BP) control is poor or lacking.
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Alzheimer's disease (AD) is conceptualized as a progressive consequence of two hallmark pathological changes in grey matter: extracellular amyloid plaques and neurofibrillary tangles.
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The adult quiescent blood-brain barrier (BBB), a structure organised by endothelial cells through interactions with pericytes, astrocytes, neurons and microglia in the neurovascular unit, is highly regulated but fragile at the same time.
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The blood-brain barrier (BBB) has been a great hurdle for brain drug delivery.
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Subcortical small-vessel disease (SSVD) is a disorder well characterized from the clinical, imaging, and neuropathological viewpoints.
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Large artery stiffness is a frequent condition that arises with ageing, and is accelerated by the presence of co-morbidities like hypertension, obesity and diabetes.
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Amyloid plaques, consisting of deposited beta-amyloid (Aβ), are a neuropathological hallmark of Alzheimer's Disease (AD).
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Brain capillary endothelial cells form the blood-brain barrier (BBB), which is covered with basement membranes and is also surrounded by pericytes and astrocyte end-feet in the neurovascular unit.
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41/100
Cerebral amyloid angiopathy (CAA) has never been more relevant.
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Sporadic cerebral amyloid angiopathy is a common, well-defined small vessel disease and a largely untreatable cause of intracerebral haemorrhage and contributor to age-related cognitive decline.
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Cerebral blood flow (CBF) regulation is essential for normal brain function.
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38/100
Amyloid-related imaging abnormalities (ARIA) in magnetic resonance imaging scans have emerged as indicators of potentially serious side effects in clinical trials of therapeutics for Alzheimer's disease.
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The 88 patients with AD included 15 with microbleeds only in cortical/subcortical regions (cortical microbleeds) that could be CAA-related, 16 with microbleeds only in deep locations (deep microbleeds), 3 with microbleeds in both cortical and deep locations (mixed microbleeds), and 54 without microbleeds.
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Verubecestat is a potent BACE1 enzyme inhibitor currently being investigated in Phase III trials for the treatment of mild-to-moderate and prodromal Alzheimer's disease.
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We show that the glymphatic fluid transporting system contributes to the delivery of choroid plexus/CSF-derived human apoE to neurons.
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Vascular cognitive impairment is the second most common form of dementia.
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Alzheimer's disease (AD) is a chronic neurodegenerative disorder characterized by the pathological accumulation of amyloid beta (Aβ) peptides and neurofibrillary tangles containing hyperphosphorylated neuronal tau protein.
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The prevalence of BMB is highly variable (3%-27% in the general population, 6%-80% in patients with vascular risk factors or vascular disease, and 16%-45% in patients with cognitive impairment).
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Multifactorial mechanisms underlying late-onset Alzheimer's disease (LOAD) are poorly characterized from an integrative perspective.
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36/100
Matrix metalloproteinases are versatile endopeptidases with many different functions in the body in health and disease.
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The results of this study showed global BBB leakage in patients with early AD that is associated with cognitive decline.
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Glymphatic transport, defined as cerebrospinal fluid (CSF) peri-arterial inflow into brain, and interstitial fluid (ISF) clearance, is reduced in the aging brain.
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The blood-brain barrier (BBB) is a vital boundary between neural tissue and circulating blood.
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Pericytes are vascular mural cells embedded in the basement membrane of blood microvessels.
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The lymphatic clearance pathways of the brain are different compared to the other organs of the body and have been the subject of heated debates.
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Cerebral amyloid angiopathy- related inflammation (CAA-ri) is an aggressive disease subtype of CAA with characteristic clinical and radiological findings.
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Hypertension (HTN) doubles the risk of Alzheimer’s disease (AD), but the mechanisms remain unclear.
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The theory on the glymphatic convection mechanism of cerebrospinal fluid holds that cardiac pulsations in part pump cerebrospinal fluid from the peri-arterial spaces through the extracellular tissue into the peri-venous spaces facilitated by aquaporin water channels.
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Structural and functional brain connectivity, synaptic activity, and information processing require highly coordinated signal transduction between different cell types within the neurovascular unit and intact blood-brain barrier (BBB) functions.
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Atraumatic convexal subarachnoid hemorrhage (cSAH) in elderly patients is a rare entity that has been associated with cerebral amyloid angiopathy (CAA) and intracerebral hematomas (ICH).
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Emerging studies link vascular risk factors and cerebrovascular health to the prevalence and rates of progression in Alzheimer's disease (AD).
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40/100
The glucose transporter GLUT1 at the blood-brain barrier (BBB) mediates glucose transport into the brain.
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Inflammatory cerebral amyloid angiopathy (CAA) typically affects older patients who present with acute or subacute cognitive decline, headache, behavioral change, seizures, and focal neurological deficits.
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Chronic kidney disease, defined by a decreased glomerular filtration rate or albuminuria, is recognized as a major global health burden, mainly because it is an established risk factor for cardiovascular and cerebrovascular diseases.
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The blood-brain barrier (BBB) limits entry of blood-derived products, pathogens, and cells into the brain that is essential for normal neuronal functioning and information processing.
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Matrix metalloproteinases (MMPs) are a family of enzymes able to degrade components of the extracellular matrix, which is important for normal blood-brain barrier function.
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There has been a growing need for in vitro models of neurodegenerative diseases such as Alzheimer's disease that would enable a better understanding of etiology and faster development of treatment strategies.
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Astrocytic network alterations have been reported in Alzheimer's disease (AD), but the underlying pathways have remained undefined.
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Aβ immunotherapy for Alzheimer's disease (AD) results in the removal of Aβ plaques and increased cerebral amyloid angiopathy (CAA).
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Vascular risk factors and cerebrovascular disease are common causes of dementia.
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Patients with AD have altered microvascular network in the retina (narrower retinal venules and a sparser and more tortuous retinal vessels) compared with matched nondemented controls.
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Cerebral amyloid angiopathy (CAA) is cerebrovascular amyloid deposition.
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The choroid plexus epithelium is a cuboidal cell monolayer, which produces the majority of the cerebrospinal fluid.
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The present data show that CAA plays a role in the development of microvascular lesions in the ageing brain, but cannot be considered as the most important factor in this vascular pathology, suggesting that other mechanisms also contribute importantly to the pathogenesis of microvascular changes.
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These data suggest that vascular leakage events, such as microhemorrhage, may be related to the removal of vascular Aβ.
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The glymphatic system is a recently defined brain-wide paravascular pathway for cerebrospinal fluid (CSF) and interstitial fluid (ISF) exchange that facilitates efficient clearance of solutes and waste from the brain.
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Neurovascular dysfunction contributes to Alzheimer's disease (AD).
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38/100
The aim of this report was to describe the case of an elderly patient with cerebral amyloid angiopathy and associated dementia who presented with new onset symptomatology compatible with an acute cerebrovascular event.
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The Blood-brain barrier (BBB), present at the level of the endothelium of cerebral blood vessels, selectively restricts the blood-to-brain paracellular diffusion of compounds; it is mandatory for cerebral homeostasis and proper neuronal function.
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Exosomes were identified in human CSF and their proteome is a potential new reservoir for biomarker discovery in neurological disorders such as Alzheimer's disease.
From across this tag
9 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 9. The same 9 appear here every time.
- Parenchymal border macrophages regulate the flow dynamics of the cerebrospinal fluid
- Neurovascular coupling in the normal brain and in hypertension, stroke, and Alzheimer disease
- Neurovascular Ageing and Age-Related Diseases
- The blood-brain barrier in brain homeostasis and neurological diseases
- Is Alzheimer's disease a neurodegenerative or a vascular disorder? Data, dogma, and dialectics
- The Meningeal Lymphatic System: A New Player in Neurophysiology
- A white matter disorder in dementia of the Alzheimer type: a pathoanatomical study
- Alzheimer's Disease: The Link Between Amyloid-β and Neurovascular Dysfunction
- Pericytes in Alzheimer's Disease: Novel Clues to Cerebral Amyloid Angiopathy Pathogenesis