ReviewInternational journal of molecular sciences2019
The Amyloid-Tau-Neuroinflammation Axis in the Context of Cerebral Amyloid Angiopathy.
Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- TREM2 deficiency causes region-specific brain effects in a mouse model of cerebral amyloid angiopathy.bioRxiv : the preprint server for biology · 2026Article
- Endothelial PAI-1 Drives Lead-Induced Cerebral Amyloid Angiopathy via Activation of C3Biology · 2026Article
- Choroidal-ventricular system abnormalities are linked to amyloid-β aggregation in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Deciphering the role of APOE in cerebral amyloid angiopathy: from genetic insights to therapeutic horizons.Annals of medicine · 2025Review
- Discovery of a Small Molecule TREM2 Agonist with Improved In Vitro Pharmacokinetic Profile and Validated Target Engagement.ACS medicinal chemistry letters · 2025Article
- Tau depletion diminishes vascular amyloid-related deficits in a mouse model of cerebral amyloid angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Dual-Phase C-11 PiB PET Images for Detecting Tau Pathology in Cerebral Amyloid Angiopathy.Annals of clinical and translational neurology · 2025Article
- Non-Drug and Non-Invasive Therapeutic Options in Alzheimer's Disease.Biomedicines · 2025Review
- Cerebral Amyloid Angiopathy, Dementia, and Alzheimer Neuropathologic Changes: Findings From the ACT Autopsy Cohort.Neurology · 2024Article
- Lead Acetate Exposure and Cerebral Amyloid Accumulation: Mechanistic Evaluations in APP/PS1 Mice.Environmental health perspectives · 2024Article
- Neuroinflammation in Alzheimer's disease: insights from peripheral immune cells.Immunity & ageing : I & A · 2024Review
- Genetic forms of tauopathies: inherited causes and implications of Alzheimer's disease-like TAU pathology in primary and secondary tauopathies.Journal of neurology · 2024Review
- Cerebrospinal fluid shotgun proteomics identifies distinct proteomic patterns in cerebral amyloid angiopathy rodent models and human patients.Acta neuropathologica communications · 2024Article
- Thinking outside the black box: are the brain endothelial cells the new main target in Alzheimer's disease?Neural regeneration research · 2023Review
- Amyloid-β (Aβ) immunotherapy induced microhemorrhages are associated with activated perivascular macrophages and peripheral monocyte recruitment in Alzheimer's disease mice.Molecular neurodegeneration · 2023Article
- Enhanced microglial dynamics and paucity of tau seeding in the amyloid plaque microenvironment contributes to cognitive resilience in Alzheimer's disease.bioRxiv : the preprint server for biology · 2023Article
- Cerebral amyloid angiopathy-related cardiac injury: Focus on cardiac cell death.Frontiers in cell and developmental biology · 2023Review
- Amyloid and tau PET in cerebral amyloid angiopathy-related inflammation two case reports and literature review.Frontiers in neurology · 2023Article
- Cerebral amyloid angiopathy interacts with neuritic amyloid plaques to promote tau and cognitive decline.Brain : a journal of neurology · 2022Article
- Reducing PDK1/Akt Activity: An Effective Therapeutic Target in the Treatment of Alzheimer's Disease.Cells · 2022Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. Currently, there is no clear understanding of the mechanisms underlying the contribution of CAA to neurodegeneration. Despite the fact that CAA is highly associated with the accumulation of Aβ, other types of amyloids have been shown to associate with the vasculature. Interestingly, in many cases, vascular amyloidosis has been associated with an active immune response and perivascular deposition of hyperphosphorylated tau. Despite the fact that in Alzheimer's disease (AD) a major focus of research has been the understanding of the connection between parenchymal amyloid plaques, tau aggregates in the form of neurofibrillary tangles (NFTs), and immune activation, the contribution of tau and neuroinflammation to neurodegeneration associated with CAA remains understudied. In this review, we discussed the existing evidence regarding the amyloid diversity in CAA and its relation to tau pathology and immune response, as well as the possible contribution of molecular and cellular mechanisms, previously associated with parenchymal amyloid in AD and AD-related dementias, to the pathogenesis of CAA. The detailed understanding of the "amyloid-tau-neuroinflammation" axis in the context of CAA could open the opportunity to develop therapeutic interventions for dementias associated with CAA that are currently being proposed for AD and AD-related dementias.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.