Evidence map›Paper›PMID 24279716›Full record

ArticleCNS neuroscience & therapeutics2014

Heat shock protein 70 reduces α-synuclein-induced predegenerative neuronal dystrophy in the α-synuclein viral gene transfer rat model of Parkinson's disease.

Teresa C Moloney, Rhona Hyland, Daniel O'Toole, Alexia Paucard, Deniz Kirik, Aideen O'Doherty, Adrienne M Gorman, Eilís Dowd

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing 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

24 citing papers in PubMed, 41 citations in OpenAlex.

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  13. Systemic Exosomal Delivery of shRNA Minicircles Prevents Parkinsonian Pathology.Molecular therapy : the journal of the American Society of Gene Therapy · 2019
    Article
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  15. New Developments in Genetic rat models of Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2018
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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

8 authors at 3 institutions in 2 countries.

Teresa C MoloneyDepartment of Pharmacology & Therapeutics, National University of Ireland, Galway, Ireland; National Centre for Biomedical Engineering Science (NCBES), National University of Ireland, Galway, Ireland; NCBES Galway Neuroscience Centre, National University of Ireland, Galway, Ireland.
Rhona Hyland
Daniel O'Toole
Alexia Paucard
Deniz Kirik
Aideen O'Doherty
Adrienne M Gorman
Eilís Dowd
Ollscoil na Gaillimhe – University of Galway · IENational University of Ireland · IELund University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsIt has become increasingly evident that the nigrostriatal degeneration associated with Parkinson's disease initiates at the level of the axonal terminals in the putamen, and this nigrostriatal terminal dystrophy is either caused or exacerbated by the presence of α-synuclein immunopositive neuronal inclusions. Therefore, strategies aimed at reducing α-synuclein-induced early neuronal dystrophy may slow or halt the progression to overt nigrostriatal neurodegeneration. Thus, this study sought to determine if adeno-associated virus (AAV) mediated overexpression of two molecular chaperone heat shock proteins, namely Hsp27 or Hsp70, in the AAV-α-synuclein viral gene transfer rat model of Parkinson's disease could prevent α-synuclein-induced early neuronal pathology.

methodsMale Sprague-Dawley rats were intranigrally coinjected with pathogenic (AAV-α-synuclein) and putative therapeutic (AAV-Hsp27 or AAV-Hsp70) viral vectors and were sacrificed 18 weeks postviral injection.

resultsIntranigral injection of AAV-α-synuclein resulted in significant α-synuclein accumulation in the substantia nigra and striatal terminals which led to significant dystrophy of nigrostriatal dopaminergic neurons without overt nigrostriatal neurodegeneration. Coinjection of AAV-Hsp70, but not AAV-Hsp27, significantly reduced AAV-α-synuclein-induced neuronal dystrophy.

conclusionsThese data confirm that overexpression of Hsp70 holds significant potential as a disease-modulating therapeutic approach for Parkinson's disease, with protective effects against early-onset α-synuclein-induced pathology demonstrated in the AAV-α-synuclein model.

Indexed as

Genetic Therapyalpha-SynucleinAnimalsBrainCorpus StriatumDopaminergic NeuronsGenetic VectorsGene Transfer TechniquesHSP27 Heat-Shock ProteinsHSP70 Heat-Shock ProteinsHumansMaleNeural PathwaysNeuroaxonal DystrophiesNeuronsNeuroprotective Agentsalpha-SynucleinHSP27 Heat-Shock ProteinsHSP70 Heat-Shock ProteinsNeuroprotective AgentsSNCA protein, humanGenetic therapyHeat-shock proteinsParkinson's disease

Identifiers

PMID24279716
PMCPMC6493192
OpenAlexW2052054514

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.