Evidence map›Paper›PMID 36918870›Full record

ReviewCell communication and signaling : CCS2023

Therapeutic potential of ADAM10 modulation in Alzheimer's disease: a review of the current evidence.

Mohammad Rafi Khezri, Mehdi Mohebalizadeh, Morteza Ghasemnejad-Berenji

Open access · goldFull text readVideo-Audio MediaReview
In one paragraph

Review in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

12 citing papers in PubMed, 30 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

3 authors at 1 institution in 1 country.

Mohammad Rafi KhezriStudent Research Committee, Urmia University of Medical Sciences, Sero Road, Urmia, 5715799313, Iran. Drmnkh76@gmail.com.ORCID 0000-0002-4280-0378
Mehdi MohebalizadehStudent Research Committee, Urmia University of Medical Sciences, Sero Road, Urmia, 5715799313, Iran.
Morteza Ghasemnejad-BerenjiStudent Research Committee, Urmia University of Medical Sciences, Sero Road, Urmia, 5715799313, Iran. ghasemnejad.m@umsu.ac.ir.ORCID 0000-0001-5672-9202
Urmia University · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD), the most common neurodegenerative disease worldwide, is caused by loss of neurons and synapses in central nervous system. Several causes for neuronal death in AD have been introduced, the most important of which are extracellular amyloid β (Aβ) accumulation and aggregated tau proteins. Increasing evidence suggest that targeting the process of Aβ production to reduce its deposition can serve as a therapeutic option for AD management. In this regard, therapeutic interventions shown that a disintegrin and metalloproteinase domain-containing protein (ADAM) 10, involved in non-amyloidogenic pathway of amyloid precursor protein processing, is known to be a suitable candidate. Therefore, this review aims to examine the molecular properties of ADAM10, its role in AD, and introduce it as a therapeutic target to reduce the progression of the disease. Video abstract.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesADAM10 ProteinAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesHumansMembrane ProteinsADAM10 ProteinADAM10 protein, humanAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAmyloid Precursor Protein SecretasesMembrane ProteinsADAM10Alzheimer’s diseaseAmyloid βNatural compounds

Identifiers

PMID36918870
PMCPMC10012555
OpenAlexW4324156239

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read4
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.