Evidence map›Paper›PMID 36100328›Full record

ReviewJournal of advanced research2022

CRISPR/Cas9 gene editing: New hope for Alzheimer's disease therapeutics.

Shanu Bhardwaj, Kavindra Kumar Kesari, Mahesh Rachamalla, Shalini Mani, Ghulam Md Ashraf, Saurabh Kumar Jha, Pravir Kumar, Rashmi K Ambasta, Harish Dureja, Hari Prasad Devkota and 8 more

Open access · goldAbstract readReview
In one paragraph

Review in Journal of advanced research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
5.9field-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

62 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
  2. Article
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  4. CRISPR-Based Gene Therapy for Brain Disease.Molecular neurobiology · 2026
    Review
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  7. Article
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  19. Signs of Alzheimer's Disease: Tied to Aging.International journal of molecular sciences · 2025
    Review
  20. Review

2 more citing papers are in PubMed but not listed here.

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

18 authors at 14 institutions in 11 countries.

Shanu BhardwajDepartment of Biotechnology, Delhi Technological University (Formerly DCE), Delhi 110042, India.
Kavindra Kumar KesariDepartment of Applied Physics, School of Science, Aalto University, 00076 Espoo, Finland.
Mahesh RachamallaDepartment of Biology, University of Saskatchewan, 112 Science Place, Saskatoon, SK S7N 5E2, Canada.
Shalini ManiDepartment of Biotechnology, Centre for Emerging Disease, Jaypee Institute of Information Technology, Noida, India.
Ghulam Md AshrafPre-Clinical Research Unit, King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia.
Saurabh Kumar JhaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201310, India.
Pravir KumarMolecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly DCE), Delhi 110042, India.
Rashmi K AmbastaMolecular Neuroscience and Functional Genomics Laboratory, Department of Biotechnology, Delhi Technological University (Formerly DCE), Delhi 110042, India.
Harish DurejaFaculty of Pharmaceutical Sciences, Maharshi Dayanand University, Rohtak, India.
Hari Prasad DevkotaGraduate School of Pharmaceutical Sciences, Kumamoto University, 5-1 Oe-honmachi, Kumamoto 862-0973, Japan.
Gaurav GuptaSchool of Pharmacy, Suresh Gyan Vihar University, Mahal road, Jagatpura, Jaipur, India.
Dinesh Kumar ChellappanDepartment of Life Sciences, School of Pharmacy, International Medical University, Bukit Jalil, Kuala Lumpur 57000, Malaysia.
Sachin Kumar SinghSchool of Pharmaceutical Sciences, Lovely Professional University, Phagwara-144411, Punjab, India.
Kamal DuaDiscipline of Pharmacy, Graduate School of Health, University of Technology Sydney, Sydney, NSW 2007, Australia; School of Pharmaceutical Sciences, Shoolini University of Biotechnology and Management Sciences, Solan 173229, Himachal Pradesh, India.
Janne RuokolainenDepartment of Applied Physics, School of Science, Aalto University, 00076 Espoo, Finland.
Mohammad Amjad KamalWest China School of Nursing / Institutes for Systems Genetics, Frontiers Science Center for Disease-related Molecular Network, West China Hospital, Sichuan University, Chengdu 610041, Sichuan, China; King Fahd Medical Research Center, King Abdulaziz University, P. O. Box 80216, Jeddah 21589, Saudi Arabia; Enzymoics, NSW 2770; Novel Global Community Educational Foundation, Australia.
Shreesh OjhaDepartment of Pharmacology and Therapeutics, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, 17666, United Arab Emirates. Electronic address: shreeshojha@uaeu.ac.ae.
Niraj Kumar JhaDepartment of Biotechnology, School of Engineering & Technology (SET), Sharda University, Greater Noida 201310, India. Electronic address: nirajkumarjha2011@gmail.com.
Delhi Technological University · INAalto University · FISharda University · INGyan Vihar University · INInstitute of Molecular Life Sciences · HUInternational Medical University · MYJaypee Institute of Information Technology · INKing Abdulaziz Medical City · SAKumamoto University · JPLovely Professional University · INMaharshi Dayanand University · INUnited Arab Emirates University · AEUniversity of Saskatchewan · CAUniversity of Technology Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is an insidious, irreversible, and progressive neurodegenerative health condition manifesting as cognitive deficits and amyloid beta (Aβ) plaques and neurofibrillary tangles. Approximately 50 million individuals are affected by AD, and the number is rapidly increasing globally. This review explores the role of CRISPR/Cas9 gene editing in the management of AD and its clinical manifestations. AIM OF REVIEW: This review aims to provide a deep insight into the recent progress in CRISPR/Cas9-mediated genome editing and its use against neurodegenerative disorders, specifically AD. However, we have referred to its use against parkinsons's disease (PD), Huntington's disease (HD), and other human diseases, as is one of the most promising and emerging technologies for disease treatment. KEY SCIENTIFIC CONCEPTS OF REVIEW: The pathophysiology of AD is known to be linked with gene mutations, that is, presenilin (PSEN) and amyloid beta precursor protein (APP). However, clinical trials focused at the genetic level could not meet the desired efficiency. The CRISPR/Cas9 genome editing tool is one of the most powerful technologies for correcting inconsistent genetic signatures and now extensively used for AD management. It has significant potential for the correction of undesired gene mutations associated with AD. This technology has allowed the development of empirical AD models, therapeutic lines, and diagnostic approaches for better understanding the nervous system, from in vitro to in vivo models.

Indexed as

Alzheimer DiseaseGene EditingAmyloid beta-PeptidesAmyloid beta-Protein PrecursorCRISPR-Cas SystemsHumansAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAlzheimer’s diseaseAPPCRISPR/Cas9Gene editingNeurodegenerationPresenilinTherapeutics

Identifiers

PMID36100328
PMCPMC9481950
OpenAlexW3181507805

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.