Evidence map›Paper›PMID 38764004›Full record

ReviewArchives of pharmacal research2024

Exploring molecular mechanisms, therapeutic strategies, and clinical manifestations of Huntington's disease.

Alaa Shafie, Amal Adnan Ashour, Saleha Anwar, Farah Anjum, Md Imtaiyaz Hassan

Abstract readReview
PubMed Publisher
In one paragraph

Review in Archives of pharmacal research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Programmed cell death pathways in huntington's disease: spotlight on ferroptosis and pyroptosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
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  16. 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

5 authors.

Alaa ShafieDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, PO Box 11099, 21944, Taif, Saudi Arabia.
Amal Adnan AshourDepartment of Oral and Maxillofacial Surgery and Diagnostic Sciences, Faculty of Dentistry, Taif University, PO Box 11099, 21944, Taif, Saudi Arabia.
Saleha AnwarCentre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, Jamia Nagar, New Delhi, 110025, India.
Farah AnjumDepartment of Clinical Laboratory Sciences, College of Applied Medical Sciences, Taif University, PO Box 11099, 21944, Taif, Saudi Arabia.
Md Imtaiyaz HassanCentre for Interdisciplinary Research in Basic Sciences, Jamia Millia Islamia, Jamia Nagar, New Delhi, 110025, India. mihassan@jmi.ac.in.ORCID http://orcid.org/0000-0002-3663-4940

Funding

King Salman Center for Disability Research KSRG-2023-242
6 · The paper itself

Abstract

Huntington's disease (HD) is a paradigm of a genetic neurodegenerative disorder characterized by the expansion of CAG repeats in the HTT gene. This extensive review investigates the molecular complexities of HD by highlighting the pathogenic mechanisms initiated by the mutant huntingtin protein. Adverse outcomes of HD include mitochondrial dysfunction, compromised protein clearance, and disruption of intracellular signaling, consequently contributing to the gradual deterioration of neurons. Numerous therapeutic strategies, particularly precision medicine, are currently used for HD management. Antisense oligonucleotides, such as Tominersen, play a leading role in targeting and modulating the expression of mutant huntingtin. Despite the promise of these therapies, challenges persist, particularly in improving delivery systems and the necessity for long-term safety assessments. Considering the future landscape, the review delineates promising directions for HD research and treatment. Innovations such as Clustered regularly interspaced short palindromic repeats associated system therapies (CRISPR)-based genome editing and emerging neuroprotective approaches present unprecedented opportunities for intervention. Collaborative interdisciplinary endeavors and a more insightful understanding of HD pathogenesis are on the verge of reshaping the therapeutic landscape. As we navigate the intricate landscape of HD, this review serves as a guide for unraveling the intricacies of this disease and progressing toward transformative treatments.

Indexed as

Huntingtin ProteinHuntington DiseaseAnimalsGene EditingGenetic TherapyHumansNeuroprotective AgentsOligonucleotides, AntisenseHTT protein, humanHuntingtin ProteinNeuroprotective AgentsOligonucleotides, AntisenseBiomarkersCAG-repeatsClinical trialsHuntington’s diseaseNeurodegenerative disordersTherapeutic approaches

Identifiers

What Socratic 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 Socratic graph.