Evidence map›Paper›PMID 35299077›Full record

ArticleJournal of neuroimmunology2022

L-methionine enhances neuroinflammation and impairs neurogenesis: Implication for Alzheimer's disease.

Amal Alachkar, Sudhanshu Agrawal, Melica Baboldashtian, Khawla Nuseir, Jon Salazar, Anshu Agrawal

Abstract read
In one paragraph

Article in Journal of neuroimmunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

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  20. mTOR Complex 1 Content and Regulation Is Adapted to Animal Longevity.International journal of molecular sciences · 2022
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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 2 institutions in 2 countries.

Amal AlachkarDepartment of Pharmaceutical Sciences, School of Pharmacy, University of California-Irvine, USA; Institute for Genomics and Bioinformatics, School of Information and Computer Sciences, University of California-Irvine, USA; Center for the Neurobiology of Learning and Memory, University of California-Irvine, Irvine, USA. Electronic address: aalachka@uci.edu.
Sudhanshu AgrawalDivision of Basic and Clinical Immunology, Department of Medicine, University of California Irvine, Irvine, CA 92697, USA.
Melica BaboldashtianDepartment of Pharmaceutical Sciences, School of Pharmacy, University of California-Irvine, USA.
Khawla NuseirDepartment of Clinical Pharmacy, Jordan University of Science and Technology, Irbid 22110, Jordan.
Jon SalazarDivision of Basic and Clinical Immunology, Department of Medicine, University of California Irvine, Irvine, CA 92697, USA.
Anshu AgrawalDivision of Basic and Clinical Immunology, Department of Medicine, University of California Irvine, Irvine, CA 92697, USA. Electronic address: aagrawal@uci.edu.
University of California, Irvine · USJordan University of Science and Technology · JO

Funding

The roles of neuronal primary cilia in Alzheimer's diseaseR01HL147311 · NHLBI · CHAPMAN UNIVERSITY · PI NAULI, SURYA · 2020 to 2023
$2.1M
Peripheral Immune mechanisms involved in the etiology of Alzheimer's diseaseR56AG064709 · NIA · UNIVERSITY OF CALIFORNIA-IRVINE · PI AGRAWAL, ANSHU · 2019 to 2019
$385k
NHLBI NIH HHS R01 HL147311NIA NIH HHS R56 AG064709
6 · The paper itself

Abstract

The disruption of methionine (L-MET) metabolism has been linked with neurodevelopmental disorders such as autism and schizophrenia and neurodegenerative disorders such as Alzheimer's disorder. We previously showed that repeated administration to adult mice of methionine produced impairments of cognitive deficits. Considering the decreased neurogenesis and increased molecular inflammation hypotheses of cognitive deficits in Alzheimer's, we aimed to explore whether the methionine regimen that produced cognitive deficits is associated with altered neuroinflammation, neurogenesis, or neurodegeneration. We found that repeated administration of L-MET at a dose equivalent to two-fold of daily dietary intake for seven days enhanced the activation of microglia and inflammation in the brain, and decreased neurogenesis in the hippocampus without affecting degeneration. Furthermore, sub-chronic and chronic L-MET treatment of human neuroblastoma (SH-SY5Y) inhibited cell cycle progression, an effect that was reversed by decreasing removing L-MET from the medium. These results support a role for neuroinflammation and neurogenesis in mediating the mechanism through which L-MET induces cognitive deficits. The results also uncover L-MET restriction, neuroinflammation, and neurogenesis as potential preventive and/or therapeutic targets for mental disorders associated with cognitive disorders, including schizophrenia and Alzheimer's disease.

Indexed as

Alzheimer DiseaseAnimalsHippocampusHumansInflammationMethionineMiceMicrogliaNeurogenesisNeuroinflammatory DiseasesMethionineBrainMethionineMicrogliaNeurogenesisNeuroinflammation

Identifiers

PMID35299077
PMCPMC13592503
OpenAlexW4220921222

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.