Evidence map›Paper›PMID 33918041›Full record

ReviewInternational journal of molecular sciences2021

Current Management and Therapeutic Strategies for Cerebral Amyloid Angiopathy.

Yasuteru Inoue, Yukio Ando, Yohei Misumi, Mitsuharu Ueda

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 2 pooled it
1.7field-weighted citation impact, top 13% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 2 syntheses or guidelines pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  6. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Yasuteru InoueDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.ORCID 0000-0003-4180-5908
Yukio AndoDepartment of Amyloidosis Research, Nagasaki International University, Sasebo 859-3298, Japan.
Yohei MisumiDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Mitsuharu UedaDepartment of Neurology, Graduate School of Medical Sciences, Kumamoto University, Kumamoto 860-8556, Japan.
Kumamoto University · JPNagasaki International University · JP

Funding

Daiwa Health Foundation noneGrants-in-Aid for Young Scientists from the Japan Society for the Promotion of Science (JSPS) 19K16919Kanae Foundation for Life & Socio-Medical Science noneKobayashi Magobe Memorial Medical Foundation noneMochida Memorial Foundation for Medical and Pharmaceutical Research nonePromotion of Joint International Research (Fostering Joint International Research (A)) from the JSPS 19KK0410SENSHIN Medical Research Foundation noneTakeda Science Foundation noneThe Japan Foundation of Applied Enzymology noneThe Osaka Medical Research Foundation for Intractable Diseases noneThe Uehara Memorial Foundation none
6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) is characterized by accumulation of amyloid β (Aβ) in walls of leptomeningeal vessels and cortical capillaries in the brain. The loss of integrity of these vessels caused by cerebrovascular Aβ deposits results in fragile vessels and lobar intracerebral hemorrhages. CAA also manifests with progressive cognitive impairment or transient focal neurological symptoms. Although development of therapeutics for CAA is urgently needed, the pathogenesis of CAA remains to be fully elucidated. In this review, we summarize the epidemiology, pathology, clinical and radiological features, and perspectives for future research directions in CAA therapeutics. Recent advances in mass spectrometric methodology combined with vascular isolation techniques have aided understanding of the cerebrovascular proteome. In this paper, we describe several potential key CAA-associated molecules that have been identified by proteomic analyses (apolipoprotein E, clusterin, SRPX1 (sushi repeat-containing protein X-linked 1), TIMP3 (tissue inhibitor of metalloproteinases 3), and HTRA1 (HtrA serine peptidase 1)), and their pivotal roles in Aβ cytotoxicity, Aβ fibril formation, and vessel wall remodeling. Understanding the interactions between cerebrovascular Aβ deposits and molecules that accumulate with Aβ may lead to discovery of effective CAA therapeutics and to the identification of biomarkers for early diagnosis.

Indexed as

AnimalsBiomarkersCerebral Amyloid AngiopathyCerebral HemorrhageClinical Decision-MakingDisease ManagementDisease SusceptibilityFluorescent Antibody TechniqueHumansImmunohistochemistryProteomeProteomicsBiomarkersProteomeamyloid βcerebral amyloid angiopathycerebral microbleedsintracerebral hemorrhageproteomic analysessuperficial siderosis

Identifiers

PMID33918041
PMCPMC8068954
OpenAlexW3147421655

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.