Evidence map›Paper›PMID 30374780›Full record

ArticleJournal of molecular neuroscience : MN2018

Preventive Effect of Two New Neurotensin Analogues on Parkinson's Disease Rat Model.

Maria Lazarova, Andrey Popatanasov, Radoslav Klissurov, Svetlana Stoeva, Tamara Pajpanova, Reni Kalfin, Lyubka Tancheva

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2018. 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
1.0field-weighted citation impact, top 28% 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, 19 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. The Emerging Role of Neuropeptides in Parkinson's Disease.Frontiers in aging neuroscience · 2021
    Review
  5. Article
  6. Protective Effect of Compound Formula Rehmannia against Neurotoxicity and Apoptosis Induced byEvidence-based complementary and alternative medicine : eCAM · 2020
    Article
  7. 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

7 authors at 2 institutions in 2 countries.

Maria LazarovaInstitute of Neurobiology, Bulgarian Academy of Sciences, Acad. G. Bonchev Str., bl. 23, 1113, Sofia, Bulgaria.
Andrey PopatanasovInstitute of Neurobiology, Bulgarian Academy of Sciences, Acad. G. Bonchev Str., bl. 23, 1113, Sofia, Bulgaria.
Radoslav KlissurovMedical University of Sofia, 2 Zdrave Str., 1000, Sofia, Bulgaria.
Svetlana StoevaInstitute of Neurobiology, Bulgarian Academy of Sciences, Acad. G. Bonchev Str., bl. 23, 1113, Sofia, Bulgaria.
Tamara PajpanovaInstitute of Molecular Biology "Roumen Tsanev", Bulgarian Academy of Sciences, Acad. G. Bonchev Str., bl. 21, 1113, Sofia, Bulgaria.ORCID http://orcid.org/0000-0001-6278-1816
Reni KalfinInstitute of Neurobiology, Bulgarian Academy of Sciences, Acad. G. Bonchev Str., bl. 23, 1113, Sofia, Bulgaria.
Lyubka TanchevaInstitute of Neurobiology, Bulgarian Academy of Sciences, Acad. G. Bonchev Str., bl. 23, 1113, Sofia, Bulgaria. lyubkatancheva@gmail.com.
Bulgarian Academy of Sciences · BGMedical University of Sofia · BG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Close functional and anatomical interactions between the neurotensin (NT) and dopamine (DA) systems suggest that NT could be associated with Parkinson's Disease (PD). However, clinical use of NT is limited due to its rapid degradation. This has led to the synthesis of a number of new NT fragment 8-13 [NT(8-13)] analogues, such as NT2 and NT4, to avoid the fast biodegradation of NT. The aim of this study was to investigate the neuroprotective effects of NT2 and NT4 on an experimental model of Parkinson's disease in rats induced with 6-hydroxydopamine (6-OHDA) treatment, producing striatal lesions. Wistar male rats were divided into different groups: a sham-operated (SO) group, a striatal 6-OHDA-lesioned control group, two groups of 6-OHDA-lesioned rats treated for 5 days with NT2 or NT4 (10 mg/kg, intraperitoneally) and a NT-treated group as reference. During the first and second week post lesion the animals were subjected to a number of behavioral tests (apomorphine-induced rotations, rotarod, passive avoidance test), and brain tissue was evaluated histologically and also assessed for DA levels. The results showed that both the number of apomorphine-induced rotations and falls (rotarod test) increased in the 6-OHDA group relative to the SO group. At the same time, the 6-OHDA-treated group showed significant memory impairment, based on the to step-through test, compared to the SO group. Treatment with NT2 and NT4 significantly decreased the number of apomorphine-induced rotations and improved the memory of lesioned animals, with these NT analogues demonstrating better neuroprotective and neuromodulatory effects than NT. DA content in the brain of the PD rats treated with NT2 and NT4 increased, possibly due to attenuation of the loss of DA-ergic neurons. NT2 and NT4 were found to easily penetrate the blood-brain barrier and they showed a better stability than the reference NT neuropeptide. In conclusion, the NT approach represents an attractive strategy for the treatment of neurodegenerative disease.

Indexed as

AnimalsBlood-Brain BarrierMaleNeuroprotective AgentsNeurotensinOxidopamineParkinson DiseasePeptide FragmentsRatsRats, WistarNeuroprotective AgentsNeurotensinOxidopaminePeptide Fragments6-OHDANeuropeptidesNeuroprotectionNeurotensinParkinson’s disease

Identifiers

PMID30374780
OpenAlexW2899278991

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.