Evidence map›Paper›PMID 33089409›Full record

ReviewNeurology and therapy2020

CRISPR-Cas9: A Promising Genome Editing Therapeutic Tool for Alzheimer's Disease-A Narrative Review.

Nirmal Chandra Barman, Niuz Morshed Khan, Maidul Islam, Zulkar Nain, Rajib Kanti Roy, Anwarul Haque, Shital Kumar Barman

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neurology and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-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

31 citing papers in PubMed, 55 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

7 authors at 4 institutions in 2 countries.

Nirmal Chandra BarmanDepartment Biotechnology and Genetic Engineering, Faculty of Biological Sciences, Islamic University, Kushtia, 7003, Bangladesh. nirmal.bge@gmail.com.ORCID http://orcid.org/0000-0002-5400-0116
Niuz Morshed KhanBiotechnology and Genetic Engineering Discipline, Khulna University, Khulna, 9208, Bangladesh.
Maidul IslamDepartment of Biotechnology and Genetic Engineering, Mawlana Bhashani Science and Technology University, Tangail, 1902, Bangladesh.
Zulkar NainDepartment Biotechnology and Genetic Engineering, Faculty of Biological Sciences, Islamic University, Kushtia, 7003, Bangladesh.
Rajib Kanti RoyDepartment of Nutrition and Food Technology, Jashore University of Science and Technology, Jashore, 7408, Bangladesh.
Anwarul HaqueDepartment Biotechnology and Genetic Engineering, Faculty of Biological Sciences, Islamic University, Kushtia, 7003, Bangladesh.
Shital Kumar BarmanSchool of Science, Western Sydney University, Locked Bag 1797, Penrith, NSW, 2751, Australia.
Islamic University · BDKhulna University · BDMawlana Bhashani Science and Technology University · BDWestern Sydney University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a chronic and irreversible neurodegenerative disorder characterized by cognitive deficiency and development of amyloid-β (Aβ) plaques and neurofibrillary tangles, comprising hyperphosphorylated tau. The number of patients with AD is alarmingly increasing worldwide; currently, at least 50 million people are thought to be living with AD. The mutations or alterations in amyloid-β precursor protein (APP), presenilin-1 (PSEN1), or presenilin-2 (PSEN2) genes are known to be associated with the pathophysiology of AD. Effective medication for AD is still elusive and many gene-targeted clinical trials have failed to meet the expected efficiency standards. The genome editing tool clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 has been emerging as a powerful technology to correct anomalous genetic functions and is now widely applied to the study of AD. This simple yet powerful tool for editing genes showed the huge potential to correct the unwanted mutations in AD-associated genes such as APP, PSEN1, and PSEN2. So, it has opened a new door for the development of empirical AD models, diagnostic approaches, and therapeutic lines in studying the complexity of the nervous system ranging from different cell types (in vitro) to animals (in vivo). This review was undertaken to study the related mechanisms and likely applications of CRISPR-Cas9 as an effective therapeutic tool in treating AD.

Indexed as

Alzheimer’s disease (AD)Clinical trialCRISPR-Cas9Genome editingTherapeutic tool

Identifiers

PMID33089409
PMCPMC7606404
OpenAlexW3094036176

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.