Evidence map›Paper›PMID 38463115›Full record

ReviewAnnals of medicine and surgery (2012)2024

Role and application of CRISPR-Cas9 in the management of Alzheimer's disease.

Nilay Soni, Indrani Kar, Jadav Dhruvkumar Narendrasinh, Sanjay Kumar Shah, Lohini Konathala, Nadine Mohamed, Meet Popatbhai Kachhadia, Mitul Hareshkumar Chaudhary, Vyapti A Dave, Lakshya Kumar and 2 more

Abstract readReview
In one paragraph

Review in Annals of medicine and surgery (2012), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
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

12 authors.

Nilay SoniDepartment of General Medicine, M. P. Shah medical college, Jamnagar.
Indrani KarDepartment of General Medicine, Lady Hardinge Medical College, University of Delhi.
Jadav Dhruvkumar NarendrasinhDepartment of General Medicine, Pandit Deendayal Upadhyay Medical College, Rajkot.
Sanjay Kumar ShahDepartment of General Medicine, Janaki Medical College, Janakpur, Nepal.
Lohini KonathalaDr NTR University of Health Sciecnes, Vijayawada, Andhra Pradesh, India.
Nadine MohamedDepartment of General Medicine, Southern Illinois University, Memorial of Carbondale Hospital, IL.
Meet Popatbhai KachhadiaDepartment of General Medicine, Pandit Deendayal Upadhyay Medical College, Rajkot.
Mitul Hareshkumar ChaudharyDepartment of General Medicine, AMA School of Medicine, Makati, Philippines.
Vyapti A DaveDepartment of General Medicine, Gujarat Medical Education and Research Society, GMERS Valsad, Gujarat.
Lakshya KumarDepartment of General Medicine, Pandit Deendayal Upadhyay Medical College, Rajkot.
Leeda AhmadiDepartment of General Medicine, Lady Hardinge medical College, New Delhi.
Varshitha GollaDepartment of General Medicine, International School of Medicine (ISM), Bishkek, Kyrgyzstan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a serious health issue that has a significant social and economic impact worldwide. One of the key aetiological signs of the disease is a gradual reduction in cognitive function and irreversible neuronal death. According to a 2019 global report, more than 5.8 million people in the United States (USA) alone have received an AD diagnosis, with 45% of those people falling into the 75-84 years age range. According to the predictions, there will be 15 million affected people in the USA by 2050 due to the disease's steadily rising patient population. Cognitive function and memory formation steadily decline as a result of an irreversible neuron loss in AD, a chronic neurodegenerative illness. Amyloid-beta and phosphorylated Tau are produced and accumulate in large amounts, and glial cells are overactive. Additionally, weakened neurotrophin signalling and decreased synapse function are crucial aspects of AD. Memory loss, apathy, depression, and irritability are among the primary symptoms. The aetiology, pathophysiology, and causes of both cognitive decline and synaptic dysfunction are poorly understood despite extensive investigation. CRISPR/Cas9 is a promising gene-editing technique since it can fix certain gene sequences and has a lot of potential for treating AD and other human disorders. Regardless of hereditary considerations, an altered Aβ metabolism is frequently seen in familial and sporadic AD. Therefore, since mutations in the PSEN-1, PSEN-2 and APP genes are a contributing factor to familial AD, CRISPR/Cas9 technology could address excessive Aβ production or mutations in these genes. Overall, the potential of CRISPR-Cas9 technology outweighs it as currently the greatest gene-editing tool available for researching neurodegenerative diseases like AD.

Indexed as

Alzheimer’s diseaseCRISPR-Cas9gene editing

Identifiers

PMID38463115
PMCPMC10923336

What OpenQuestion holds

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Registered trials

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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.