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amyloid-angiopathy
229 studies tagged amyloid-angiopathy, 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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Cerebral small vessel disease (cSVDs) account for 25% of stroke and are a frequent cause of cognitive or motor disability in adults.
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BBBO was achieved in 5 out of 6 subjects with an average volume of 983±626 mm 3 following FUS at the right frontal lobe both in white and gray matter regions.
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This editorial summarizes advances from the Clearance of Interstitial Fluid and Cerebrospinal Fluid (CLIC) group, within the Vascular Professional Interest Area (PIA) of the Alzheimer's Association International Society to Advance Alzheimer's Research and Treatment (ISTAART).
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We found non-significant differences in age (F(2, 141) = 1.304; P = 0.275) and years of education (F(2, 141) = 0.013; P = 0.987).
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The increase in blood flow evoked by whisker stimulation (functional hyperemia) or by endothelial and smooth muscle vasoactivity was markedly attenuated in WT → Tg2576 chimeras but was fully restored in CD36-/- → Tg2576 chimeras, in which BAM ROS production was suppressed.
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Cerebral amyloid angiopathy (CAA) is an important cerebral small vessel disease associated with brain haemorrhage and cognitive change.
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Cerebral small vessel disease is a neurological disease that affects the brain microvasculature and which is commonly observed among the elderly.
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Our study establishes a connection between Aβ antibodies engaged at CAA deposits, the activation of perivascular macrophages, and the upregulation of genes involved in vascular permeability.
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Vascular cognitive impairment (VCI) is a lifelong process encompassing a broad spectrum of cognitive disorders, ranging from subtle or mild deficits to prodromal and fully developed dementia, originating from cerebrovascular lesions such as large and small vessel disease.
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Cerebral amyloid angiopathy-related inflammation (CAA-RI) is an encephalopathy caused by inflammation of β-amyloid peptide deposition in cerebrovascular vessels.
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White matter hyperintensities (WMH) - - areas of increased signal appearing on T2-weighted magnetic resonance imaging - - are associated with Alzheimer’s disease (AD) risk and progression in late onset and genetic forms.
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54/100
Cerebrovascular dysregulation is a hallmark of Alzheimer's disease (AD), but the changes that occur in specific cell types have not been fully characterized.
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Dilation of perivascular spaces (PVS) in the brain may indicate poor fluid drainage due to the accumulation of perivascular cell debris, waste, and proteins, including amyloid-beta (Aβ).
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Reducing the levels of APOE4 in astrocytes shifted the deposition of fibrillar Aβ from the brain parenchyma to the cerebrovasculature.
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41/100
Vascular cognitive impairment (VCI) refers to all forms of cognitive disorder related to cerebrovascular diseases, including vascular mild cognitive impairment, post-stroke dementia, multi-infarct dementia, subcortical ischemic vascular dementia (SIVD), and mixed dementia.
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The blood-brain barrier (BBB) protects the brain but is also an important obstacle for the effective delivery of therapeutics in Alzheimer's disease and other neurodegenerative disorders.
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Cerebral endothelial cells and their linking tight junctions form a unique, dynamic and multi-functional interface, the blood-brain barrier (BBB).
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The cerebral vascular system stringently regulates cerebral blood flow (CBF).
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Amyloid β (Aβ) peptide is deposited in the brains of sporadic Alzheimer's disease (AD) due to impaired vessel-dependent clearance.
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Alzheimer's disease (AD) is the most common cause of dementia and is characterized by progressive neurodegeneration and cognitive decline.
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Macrophages are important players in the maintenance of tissue homeostasis 1 .
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Decades of research into anti-Aβ immunotherapies provide evidence for increased Aβ clearance from the brain; however, this is frequently accompanied by complicated vascular deficits.
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Acute ischemic cardiac injury predisposes one to cognitive impairment, dementia, and depression.
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This scientific commentary refers to ‘Cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline’ by Rabin et al. (https://doi.org/10.1093/brain/awac178).
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Cerebral small vessel disease (CSVD) represents a diverse cluster of cerebrovascular diseases primarily affecting small arteries, capillaries, arterioles and venules.
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β-amyloid (Aβ) deposits in brain blood vessel walls underlie the vascular pathology of Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA).
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Cerebral amyloid angiopathy (CAA) is a small vessel disease characterized by amyloid β (Aβ) peptide deposition within the walls of medium to small-caliber blood vessels, cerebral microhemorrhage, and blood-brain barrier (BBB) leakage.
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We studied small vessel disease (SVD) pathology in Familial Alzheimer's disease (FAD) subjects carrying the presenilin 1 (PSEN1) p.Glu280Ala mutation in comparison to those with sporadic Alzheimer's disease (SAD) as a positive control for Alzheimer's pathology and Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) bearing different NOTCH3 mutations, as positive controls for SVD pathology.
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High-speed high-resolution imaging of the whole-brain hemodynamics is critically important to facilitating neurovascular research.
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The mechanism whereby an increase in neuronal activity (NA) leads to a local elevation in cerebral blood flow to supply the active neurons with oxygen and nutrients and remove the catabolic waste has been termed neurovascular coupling (NVC).
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Cerebral small vessel disease (cSVD) is a major cause of stroke and dementia.
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Blood-brain-barrier (BBB) dysfunction is a hallmark of aging and aging-related disorders, including cerebral small vessel disease and Alzheimer's disease.
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We observe a 3.71-fold increase in BACE1 expression in the cerebral microvessels from patients with hypertension.
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Small vessel disease (SVD) is one of the most frequent pathological conditions which lead to dementia.
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rTg-D rats begin to accumulate Aβ in brain and develop varying levels of larger vessel CAA type-2, in the absence of capillary CAA type-1, starting around 18 months of age.
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The human brain vasculature is of great medical importance: its dysfunction causes disability and death 1 , and the specialized structure it forms-the blood-brain barrier-impedes the treatment of nearly all brain disorders 2,3 .
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There is an increasing prevalence of Vascular Cognitive Impairment (VCI) worldwide, and several studies have suggested that Chronic Cerebral Hypoperfusion (CCH) plays a critical role in disease onset and progression.
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An accurate diagnosis of sporadic cerebral amyloid angiopathy (CAA) is critical for patient management and research (including clinical trials) for this common small vessel pathology of the brain.
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Perivascular spaces (PVS) are compartments surrounding cerebral blood vessels that become visible on MRI when enlarged.
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Cerebral microbleeds (CMBs) are a disorder of cerebral microvessels that are characterized as small (<10 mm), hypointense, round or ovoid lesions seen on T2*-weighted gradient echo MRI.
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Alterations in cerebral blood flow are common in several neurological diseases among the elderly including stroke, cerebral small vessel disease, vascular dementia, and Alzheimer's disease. 4D flow magnetic resonance imaging (MRI) is a relatively new technique to investigate cerebrovascular disease, and makes it possible to obtain time-resolved blood flow measurements of the entire cerebral arterial venous vasculature and can be used to derive a repertoire of hemodynamic biomarkers indicative of cerebrovascular health.
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Vascular dementia (VaD) constitutes the second most prevalent cause of dementia in the world after Alzheimer's disease (AD).
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41/100
Alzheimer's disease (AD) is clinically characterized by a progressive loss of cognitive functions and short-term memory.
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Alzheimer's disease (AD) and cerebral small vessel disease (cSVD) are the two main causes of dementia with blood-brain barrier (BBB) breakdown being a common contributor.
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Increased cerebrovascular amyloid-β (Aβ) deposition represents the main pathogenic mechanisms characterizing Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA).
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41/100
Vascular dementia is the second leading cause of dementia after Alzheimer's disease in the elderly population worldwide.
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Our analyses demonstrate lower retinal capillary densities in early disease, in cognitively normal APOE ε4 gene carriers.
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The breath-holding index was reduced in the AD continuum and was inversely correlated to CSF amyloid β42 levels.
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Reliable quantitative blood biomarkers are important in vascular dementia (VaD) because early diagnosis and therapeutic intervention are effective in preventing progression of dementia.
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40/100
Brain function critically depends on a close matching between metabolic demands, appropriate delivery of oxygen and nutrients, and removal of cellular waste.
From across this tag
8 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 8. The same 8 appear here every time.
- Aging and cerebrovascular disease
- The Meningeal Lymphatic System: A New Player in Neurophysiology
- Brain endothelial Gαq/11 signalling in cerebrovascular function and cognition of aged mice
- Perivascular nerves and the regulation of cerebrovascular tone
- Emerging concepts in sporadic cerebral amyloid angiopathy
- Blood-brain barrier penetration and in vivo activity of an NGF conjugate
- Early Binding of Anti-Amyloid Antibodies to CAA Drives Complement Activation, Inflammation and ARIA in Mice
- Tight junctions at the blood brain barrier: physiological architecture and disease-associated dysregulation