Evidence map›Paper›PMID 38104040›Full record

ArticleNeurochemical research2024

Memantine Improves Memory and Neurochemical Damage in a Model of Maple Syrup Urine Disease.

Isabela da Silva Lemos, Carolina Antunes Torres, Carolina Giassi Alano, Rafaela Tezza Matiola, Rejane de Figueiredo Seldenreich, Alex Paulo Zeferino Padilha, Ellen De Pieri, Pauline Souza Effting, Ricardo Andrez Machado-De-Ávila, Gislaine Zilli Réus and 2 more

Abstract read
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Article in Neurochemical research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. 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

12 authors at 2 institutions in 1 country.

Isabela da Silva LemosPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Doenças Neurometabólicas, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0000-0003-1715-7488
Carolina Antunes TorresPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Doenças Neurometabólicas, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0009-0000-8743-0713
Carolina Giassi AlanoPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Doenças Neurometabólicas, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0000-0001-8710-036X
Rafaela Tezza MatiolaPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Doenças Neurometabólicas, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0000-0002-5384-1220
Rejane de Figueiredo SeldenreichPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Doenças Neurometabólicas, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0000-0001-5821-4405
Alex Paulo Zeferino PadilhaPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Psiquiatria Translacional, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0009-0003-5068-9299
Ellen De PieriPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0000-0002-2449-1225
Pauline Souza EfftingPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Doenças Neurometabólicas, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0000-0002-1746-8289
Ricardo Andrez Machado-De-ÁvilaPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0000-0002-1303-0490
Gislaine Zilli RéusPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Psiquiatria Translacional, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil.ORCID http://orcid.org/0000-0001-6073-0855
Guilhian LeipnitzPrograma de Pós-graduação em Ciências Biológicas: Bioquímica, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, 90035-003, Brazil.ORCID http://orcid.org/0000-0001-7964-8923
Emilio Luiz StreckPrograma de Pós-graduação em Ciências da Saúde, Laboratório de Doenças Neurometabólicas, Universidade do Extremo Sul Catarinense, Criciúma, SC, 88806-000, Brazil. emiliostreck@gmail.com.ORCID http://orcid.org/0000-0002-2859-4678
Universidade do Extremo Sul Catarinense · BRUniversidade Federal do Rio Grande do Sul · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maple Syrup Urine Disease (MSUD) is a metabolic disease characterized by the accumulation of branched-chain amino acids (BCAA) in different tissues due to a deficit in the branched-chain alpha-ketoacid dehydrogenase complex. The most common symptoms are poor feeding, psychomotor delay, and neurological damage. However, dietary therapy is not effective. Studies have demonstrated that memantine improves neurological damage in neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. Therefore, we hypothesize that memantine, an NMDA receptor antagonist can ameliorate the effects elicited by BCAA in an MSUD animal model. For this, we organized the rats into four groups: control group (1), MSUD group (2), memantine group (3), and MSUD + memantine group (4). Animals were exposed to the MSUD model by the administration of BCAA (15.8 µL/g) (groups 2 and 4) or saline solution (0.9%) (groups 1 and 3) and treated with water or memantine (5 mg/kg) (groups 3 and 4). Our results showed that BCAA administration induced memory alterations, and changes in the levels of acetylcholine in the cerebral cortex. Furthermore, induction of oxidative damage and alterations in antioxidant enzyme activities along with an increase in pro-inflammatory cytokines were verified in the cerebral cortex. Thus, memantine treatment prevented the alterations in memory, acetylcholinesterase activity, 2',7'-Dichlorofluorescein oxidation, thiobarbituric acid reactive substances levels, sulfhydryl content, and inflammation. These findings suggest that memantine can improve the pathomechanisms observed in the MSUD model, and may improve oxidative stress, inflammation, and behavior alterations.

Indexed as

Maple Syrup Urine DiseaseAcetylcholinesteraseAmino Acids, Branched-ChainAnimalsAntioxidantsDisease Models, AnimalInflammationMemantineRatsAcetylcholinesteraseAmino Acids, Branched-ChainAntioxidantsMemantinebranched-chain amino acidsCholinergic systemHigh leucineInflammationOxidative stress

Identifiers

PMID38104040
OpenAlexW4389841745

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.