Evidence map›Paper›PMID 33659724›Full record

ReviewHeliyon2021

Harleen Kohli, Pravir Kumar, Rashmi K Ambasta

Open access · goldAbstract readReview
In one paragraph

Review in Heliyon, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021
    Review
  5. Article
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

3 authors at 1 institution in 1 country.

Harleen KohliMolecular Neuroscience and Functional Genomics Laboratory, Delhi Technological University (Formerly Delhi College of Engineering), Delhi 110042, India.
Pravir KumarMolecular Neuroscience and Functional Genomics Laboratory, Delhi Technological University (Formerly Delhi College of Engineering), Delhi 110042, India.
Rashmi K AmbastaMolecular Neuroscience and Functional Genomics Laboratory, Delhi Technological University (Formerly Delhi College of Engineering), Delhi 110042, India.
Delhi Technological University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease is a neurodegenerative disease caused by CAG repeat in the first exon of HTT (Huntingtin) gene, leading to abnormal form of Htt protein containing enlarged polyglutamine strands of variable length that stick together to form aggregates and is toxic to brain causing brain damage. Complete reversal of brain damage is not possible till date but recovery may be possible by peptide therapy. The peptide-based therapy for Huntington's disease includes both poly Q peptide as well as non poly Q peptides like (QBP1)2, p42, Exendin 4, ED11, CaM, BiP, Leuprorelin peptide. The novel approach that is currently being tested in this article is the peptide-based therapy to target the mutated protein. This approach is based on the principle of preventing the aggregation of mutant Htt by blocking the potential sites responsible for protein aggregation and thereby ameliorating the disease symptoms. Herein, we have screened a variety of potential peptides that were known to prevent the protein aggregation, comparatively analyzed their binding affinity with homology modeled Htt protein, designed novel peptides based upon conservation analysis among screened potential peptides as a therapeutic agent, comparatively analyzed the therapeutic potential of novel peptides against modeled Htt protein for investigating the therapeutic prospects of Huntington's disease. We have designed a peptide for the therapy of Huntington's disease by comparing several peptides, which are already in use for Huntington's disease.

Indexed as

Htt proteinHuntington's diseaseNeurodegenerative diseasePeptide-based therapyPolyglutamine disorders

Identifiers

PMID33659724
PMCPMC7890153
OpenAlexW3132515409

What OpenQuestion 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 OpenQuestion graph.