Tier 3 — preclinical

Betaine suppressed Aβ generation by altering amyloid precursor protein processing

Xiu-Ping Liu, Xiang Qian, Yue Xie, Yan Qi, Min-Feng Peng, Bi-Cui Zhan, Zheng-Qing Lou
Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 2014 35(7):1009-1013

Bibliography

PubMed
PMID 24549986
DOI
10.1007/s10072-014-1630-y
Funding
Funding was not specified in the indexed record or accessible funding metadata.
Competing interests
A competing-interest declaration was not available in the indexed record or accessible disclosure metadata.

Study snapshot

DesignExperimental animal and/or laboratory research
ModelAPP-mutant N2a cells
SampleExperiment-specific biological replicates and model groups; see original methods
InterventionBetaine treatment in cultured cells
DurationIn vitro exposure
EndpointsAPP processing; Amyloid-beta

What the study showed, in plain terms

Published in 2014, 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 Betaine treatment in cultured cells. Follow-up or treatment period: In vitro exposure.

Betaine reduced measured amyloid-beta production and shifted secretase-related APP processing in the cell model.

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 reduced measured amyloid-beta production and shifted secretase-related APP processing in the cell model.
  • The recorded outcome domains were APP processing; Amyloid-beta.
  • The result applies to the tested exposure: Betaine treatment in cultured cells; In vitro exposure.

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