Evidence map›Paper›PMID 38078920›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2024

Gene therapy: an alternative to treat Alzheimer's disease.

Vanshika Doshi, Garima Joshi, Sanjay Sharma, Deepak Choudhary

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

7 citing papers in PubMed, 11 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

4 authors at 2 institutions in 1 country.

Vanshika DoshiShobhaben Pratapbhai Patel School of Pharmacy & Technology Management, SVKM's NMIMS (Deemed to be University), Vile Parle West, Mumbai, Maharashtra, 400056, India.
Garima JoshiDepartment of Pharmaceutical Sciences, Mohanlal Sukhadia University, Udaipur, Rajasthan, 313001, India.
Sanjay SharmaShobhaben Pratapbhai Patel School of Pharmacy & Technology Management, SVKM's NMIMS (Deemed to be University), Vile Parle West, Mumbai, Maharashtra, 400056, India. sanjaysharma.qa@gmail.com.
Deepak ChoudharyDepartment of Pharmaceutical Sciences, Mohanlal Sukhadia University, Udaipur, Rajasthan, 313001, India. deepakseervi@gmail.com.
Mohanlal Sukhadia University · INNarsee Monjee Institute of Management Studies · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD), a neuro-degenerative disease that primarily affects the elderly, is a worldwide phenomenon. Loss of memory, cognitive decline, behavioural changes, and many other signs are used to classify it. Various hypotheses that may contribute to Alzheimer's disease have been found during decades of survey, including tau theory, the amyloid theory, the cholinergic hypothesis, and the oxidative stress hypothesis. According to some theories, the two leading causes of AD are the accumulation of amyloid beta plaque and development of NFTs in the brain. The hippocampus and cerebral cortex are the primary sites where amyloid beta plaques gather in the body. NFT formation in the brain impairs the brain's neurons' potential of signalling. According to the age at which it manifests in a person, there are two subtypes of AD: 'LOAD (Late Onset Alzheimer's Disease)' and 'EOAD (Early Onset Alzheimer's Disease)'. Long-term research into AD treatment has resulted in the introduction of some medications that provided symptomatic relief to patients but did not alter the disease's pathophysiology, like cholinesterase inhibitors, inhibitors of tau aggregation, and monoclonal antibodies to Aβ aggregation. Even though the medications did not halt the progression of AD, researchers did not discontinue their work, which lead to the introduction of gene therapy - a recently created cutting-edge method of delivering genes to target sites where they can express the intended functionalities. Viral or non-viral vectors could be used to deliver the gene, each with advantages and limitations of their own. Gene therapy is proven to be a potential disease-modifying treatment for AD. This article discusses about gene therapy, its merits and demerits and the various ways of gene delivery. Additionally, it focuses on AD as the target for treatment through gene therapy, the pathophysiology of AD, and the multiple targets for gene therapy in the treatment of AD.

Indexed as

Alzheimer DiseaseGenetic TherapyAmyloid beta-PeptidesAnimalsHumansAmyloid beta-PeptidesAlzheimer’s disease (AD)Gene deliveryGene therapyHypothesisPathophysiologyTreatmentVector

Identifiers

PMID38078920
OpenAlexW4389566251

What OpenQuestion holds

Textmetadata
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.