Evidence map›Paper›PMID 37681238›Full record

ArticleDisease models & mechanisms2023

Increase in brain glycogen levels ameliorates Huntington's disease phenotype and rescues neurodegeneration in Drosophila.

Akanksha Onkar, Deepashree Sheshadri, Anupama Rai, Arjit Kant Gupta, Nitin Gupta, Subramaniam Ganesh

Open access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

8 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

6 authors at 1 institution in 1 country.

Akanksha OnkarDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology (IIT), Kanpur 208016, India.ORCID 0000-0003-0878-6450
Deepashree SheshadriDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology (IIT), Kanpur 208016, India.ORCID 0000-0001-9582-5643
Anupama RaiDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology (IIT), Kanpur 208016, India.
Arjit Kant GuptaDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology (IIT), Kanpur 208016, India.
Nitin GuptaDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology (IIT), Kanpur 208016, India.ORCID 0000-0002-8408-3848
Subramaniam GaneshDepartment of Biological Sciences and Bioengineering, Indian Institute of Technology (IIT), Kanpur 208016, India.ORCID 0000-0002-9908-9177
Indian Institute of Technology Kanpur · IN

Funding

Wellcome TrustWellcome Trust IA/I/15/2/502091
6 · The paper itself

Abstract

Under normal physiological conditions, the mammalian brain contains very little glycogen, most of which is stored in astrocytes. However, the aging brain and the subareas of the brain in patients with neurodegenerative disorders tend to accumulate glycogen, the cause and significance of which remain largely unexplored. Using cellular models, we have recently demonstrated a neuroprotective role for neuronal glycogen and glycogen synthase in the context of Huntington's disease. To gain insight into the role of brain glycogen in regulating proteotoxicity, we utilized a Drosophila model of Huntington's disease, in which glycogen synthase is either knocked down or expressed ectopically. Enhancing glycogen synthesis in the brains of flies with Huntington's disease decreased mutant Huntingtin aggregation and reduced oxidative stress by activating auto-lysosomal functions. Further, overexpression of glycogen synthase in the brain rescues photoreceptor degeneration, improves locomotor deficits and increases fitness traits in this Huntington's disease model. We, thus, provide in vivo evidence for the neuroprotective functions of glycogen synthase and glycogen in neurodegenerative conditions, and their role in the neuronal autophagy process.

Indexed as

Huntington DiseaseNeurodegenerative DiseasesAnimalsBrainDisease Models, AnimalDrosophilaGlycogen SynthaseHumansHuntingtin ProteinMammalsPhenotypeGlycogen SynthaseHuntingtin ProteinAgingAutophagyGlycogen synthaseNeurodegenerative disordersOxidative stress

Identifiers

PMID37681238
PMCPMC10602008
OpenAlexW4386530735

What OpenQuestion holds

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LicenceCC BY
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.