ReviewJournal of Alzheimer's disease reports2022
Updated Outlook of Cerebral Amyloid Angiopathy and Inflammatory Subtypes: Pathophysiology, Clinical Manifestations, Diagnosis and Management.
Review in Journal of Alzheimer's disease reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Adiponectin deficiency drives cerebrovascular dysfunction and synergizes with amyloid-β to exacerbate alzheimer's pathology.Alzheimer's research & therapy · 2026Article
- Clinical-Radiological Spectrum of Cerebral Amyloid Angiopathy-Related Inflammation.Annals of neurology · 2026Article
- Cerebrospinal fluid biomarkers in cerebral amyloid angiopathy: insights from a clinical case series.Arquivos de neuro-psiquiatria · 2025Article
- Deciphering the role of APOE in cerebral amyloid angiopathy: from genetic insights to therapeutic horizons.Annals of medicine · 2025Review
- A Case of Amyloid Beta-Related Angiitis: Rare Inflammatory Vasculopathy of the Central Nervous System.Cureus · 2025Article
- Cerebral Amyloid Angiopathy: A Case Report.Cureus · 2025Article
- Iatrogenic Dementia: Providing Insight into Transmissible Subtype of Alzheimer's Disease, Creutzfeldt-Jakob Disease and Cerebral Amyloid Angiopathy.Biomolecules · 2025Review
- Cerebral amyloid angiopathy: a narrative review.Frontiers in aging neuroscience · 2025Review
- Atherosclerotic burden and cerebral small vessel disease: exploring the link through microvascular aging and cerebral microhemorrhages.GeroScience · 2024Review
- Cerebral Amyloid Angiopathy-Related Inflammation (CAA-rI): Three Heterogeneous Case Reports and a Focused Literature Review.Brain sciences · 2023Article
- Rare forms of cerebral amyloid angiopathy: pathogenesis, biological and clinical features of CAA-ri and iCAA.Frontiers in neuroscience · 2023Review
- A Case of Severe Cerebral Amyloid Angiopathy-Related Inflammation in a 81-Year-Old Woman with Rapid Cognitive Decline.Case reports in neurologyArticle
- Retinal Vasculopathy in Inflammatory Cerebral Amyloid Angiopathy: A Case Report of Peripheral Marker of Treatment Response.Case reports in ophthalmologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cerebral amyloid angiopathy (CAA) is a common untreatable cause of lobar hemorrhages and cognitive decline in the older population. Subset of patients present with its inflammatory subtype with rapid decline in cognitive functions and neurological deficits. Most commonly the underlying pathophysiology of this disease is deposition of insoluble amyloid protein into blood vessel walls which results in vessel fragility leading to local neurotoxicity which may eventually leads to lobar hemorrhages and cognitive decline. The term "Amyloid Spell" encompasses transient focal neurological deficits which is commonly misdiagnosed as seizures or transient ischemic attack in the emergency department. Radiologic findings in these patients may reveal microbleeds, cortical superficial siderosis, white matter hyperintensities, and cerebral edema which support the clinical diagnosis which could be otherwise challenging. CAA diagnostic criteria require CT (Edinburgh Criteria) or MRI imaging, or neuropathology. The diagnosis can be suspected without imaging or neuropathology but cannot be confirmed. This review article provides a critical outlook on different types of presentations, updated diagnostic criteria and management of CAA patients illustrating underlying mechanisms associated with neuronal injury secondary to amyloid deposition.
Indexed as
Identifiers
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.