Tier 3 — preclinical

Betaine ameliorates schizophrenic traits by functionally compensating for KIF3-based CRMP2 transport

Shogo Yoshihara, Xuguang Jiang, Momo Morikawa, Tadayuki Ogawa, Sotaro Ichinose, Hirooki Yabe, Akiyoshi Kakita, Manabu Toyoshima, Yasuto Kunii, Takeo Yoshikawa, Yosuke Tanaka, Nobutaka Hirokawa
Cell reports 2021 35(2):108971

Bibliography

PubMed
PMID 33852848
DOI
10.1016/j.celrep.2021.108971
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
Reported disclosure: Declaration of interests The authors declare no competing interests.

Study snapshot

DesignExperimental animal and/or laboratory research
ModelKif3b-deficient mice and neuronal models
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionHigh-betaine diet and neuronal experiments
DurationModel-specific experimental protocols
EndpointsNeuronal morphology; CRMP2; Mouse behavior

What the study showed, in plain terms

Published in 2021, this source examined preclinical aging, brain and metabolic mechanisms. Design: Experimental animal and/or laboratory research. Sample/model: Experiment-specific biological replicates and model groups; see original methods. The exposure or intervention was High-betaine diet and neuronal experiments. Follow-up or treatment period: Model-specific experimental protocols.

Betaine improved selected schizophrenia-like mouse behaviors and neuronal morphology, with a proposed CRMP2-transport mechanism.

Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.

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Key findings

  • Betaine improved selected schizophrenia-like mouse behaviors and neuronal morphology, with a proposed CRMP2-transport mechanism.
  • The recorded outcome domains were Neuronal morphology; CRMP2; Mouse behavior.
  • The result applies to the tested exposure: High-betaine diet and neuronal experiments; Model-specific experimental protocols.

What this study can and cannot tell us

  • Experimental model evidence. The intervention, concentrations and outcomes do not establish an effective human supplement dose or a clinical treatment benefit.
  • Cell concentrations, species, disease models and experimental routes cannot be converted directly into an effective or safe oral human regimen.
  • Source basis: Indexed abstract and bibliographic data. Missing method details, funding information or participant denominators are not inferred.

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Editorial review

Reviewed by the Biohack Blueprint research team

Last verified

Dr. Khaled Mahmoud, MBBChCritical Care Medicine, Longevity Science & Editorial Direction Dr. Amr Yasser, PhDCardiometabolic, Musculoskeletal, Gut & Bioavailability Dr. Abdulla Mostafa, PhDCellular Senescence, Neurological, Mitochondrial & Brain-Ageing Biology