Evidence map›Paper›PMID 32183348›Full record

ReviewInternational journal of molecular sciences2020

Potential Therapeutic Approaches for Cerebral Amyloid Angiopathy and Alzheimer's Disease.

Masashi Tanaka, Satoshi Saito, Takayuki Inoue, Noriko Satoh-Asahara, Masafumi Ihara

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Masashi TanakaDepartment of Physical Therapy, Health Science University, 7187 Kodachi, Fujikawaguchiko-machi, Minamitsuru-gun, Yamanashi 401-0380, Japan.ORCID 0000-0003-0719-8972
Satoshi SaitoDepartment of Neurology, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan.ORCID 0000-0001-8608-058X
Takayuki InoueDepartment of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, 1-1 Fukakusa Mukaihata-cho, Fushimi-ku, Kyoto 612-8555, Japan.
Noriko Satoh-AsaharaDepartment of Endocrinology, Metabolism, and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, 1-1 Fukakusa Mukaihata-cho, Fushimi-ku, Kyoto 612-8555, Japan.
Masafumi IharaDepartment of Neurology, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan.ORCID 0000-0002-7102-4048
Kyoto Medical Center · JPNational Cerebral and Cardiovascular Center · JP

Funding

Eli Lilly Japan N/AHealth Science University N/AIntramural Research Fund (29-6-15) for Cerebrovascular Diseases of National Cerebral and Cardiovascular Center N/AJapan Society for the Promotion of Science JP17K14958Japan Society for the Promotion of Science JP18H02737Japan Society for the Promotion of Science JP18K19769Japan Society for the Promotion of Science JP19K07927Japan Society for the Promotion of Science JP19K11760Mochida Pharmaceutical Company N/ANational Hospital Organization for collaborative clinical research H26-NHO-02Smoking Research Foundation 2019T004Takeda Pharmaceutical Company N/ATakeda Science Foundation N/A
6 · The paper itself

Abstract

Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease directly implicated in Alzheimer's disease (AD) pathogenesis through amyloid-β (Aβ) deposition, which may cause the development and progression of dementia. Despite extensive studies to explore drugs targeting Aβ, clinical benefits have not been reported in large clinical trials in AD patients or presymptomatic individuals at a risk for AD. However, recent studies on CAA and AD have provided novel insights regarding CAA- and AD-related pathogenesis. This work has revealed potential therapeutic targets, including Aβ drainage pathways, Aβ aggregation, oxidative stress, and neuroinflammation. The functional significance and therapeutic potential of bioactive molecules such as cilostazol and taxifolin have also become increasingly evident. Furthermore, recent epidemiological studies have demonstrated that serum levels of a soluble form of triggering receptor expressed on myeloid cells 2 (TREM2) may have clinical significance as a potential novel predictive biomarker for dementia incidence. This review summarizes recent advances in CAA and AD research with a focus on discussing future research directions regarding novel therapeutic approaches and predictive biomarkers for CAA and AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAnimalsAspartic Acid EndopeptidasesBiomarkersBrainCerebral Amyloid AngiopathyCilostazolDisease Models, AnimalHumansMembrane GlycoproteinsMiceNeuroprotective AgentsOxidative StressProtein Aggregation, PathologicalAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanBiomarkersCilostazolMembrane GlycoproteinsNeuroprotective AgentsQuercetinReceptors, ImmunologictaxifolinTREM2 protein, humanAlzheimer’s diseaseamyloid-βantioxidantscerebral amyloid angiopathycilostazolglycationinflammationintramural peri-arterial drainagetaxifolintriggering receptor expressed on myeloid cells 2

Identifiers

PMID32183348
PMCPMC7139812
OpenAlexW3010918008

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.