ArticlePloS one2010
Lactic acid induces aberrant amyloid precursor protein processing by promoting its interaction with endoplasmic reticulum chaperone proteins.
Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Alzheimer's disease risk geneBrain communications · 2026Article
- Lens Proteomics Provide Novel Clues for Cataractogenesis: Original Investigation and a Broad Literature Survey.Journal of clinical medicine · 2025Article
- Involvement of Phosphate and the Consequences of Its High Consumption in Energy Metabolism and Muscle Functions.Journal of nutrition and metabolism · 2025Review
- Pediococcus pentosaceus LAB6- and Lactiplantibacillus plantarum LAB12-Derived Cell Free Supernatant Inhibited RhoA Activation and Reduced Amyloid-Β In Vitro.Probiotics and antimicrobial proteins · 2024Article
- The Cleavage-Specific Tau 12A12mAb Exerts an Anti-Amyloidogenic Action by Modulating the Endocytic and Bioenergetic Pathways in Alzheimer's Disease Mouse Model.International journal of molecular sciences · 2023Article
- Integrated multi-omics analysis of Huntington disease identifies pathways that modulate protein aggregation.Disease models & mechanisms · 2022Article
- The regulatory effects of lactic acid on neuropsychiatric disorders.Discover mental health · 2022Review
- Targeted Metabolomic Analysis in Alzheimer's Disease Plasma and Brain Tissue in Non-Hispanic Whites.Journal of Alzheimer's disease : JAD · 2022Article
- Gut-microbiota-microglia-brain interactions in Alzheimer's disease: knowledge-based, multi-dimensional characterization.Alzheimer's research & therapy · 2021Article
- Article
- GLUT12 Expression in Brain of Mouse Models of Alzheimer's Disease.Molecular neurobiology · 2020Article
- Lactate as a Metabolite and a Regulator in the Central Nervous System.International journal of molecular sciences · 2016Review
- Role of diffuse low-level heteroplasmy of mitochondrial DNA in Alzheimer's disease neurodegeneration.Frontiers in aging neuroscience · 2015Article
- A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome.Metabolic brain disease · 2013Review
- Adenosine monophosphate-activated protein kinase overactivation leads to accumulation of α-synuclein oligomers and decrease of neurites.Neurobiology of aging · 2013Article
- Mitochondrial dysfunction and cellular metabolic deficiency in Alzheimer's disease.Neuroscience bulletin · 2012Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundLactic acid, a natural by-product of glycolysis, is produced at excess levels in response to impaired mitochondrial function, high-energy demand, and low oxygen availability. The enzyme involved in the production of β-amyloid peptide (Aβ) of Alzheimer's disease, BACE1, functions optimally at lower pH, which led us to investigate a potential role of lactic acid in the processing of amyloid precursor protein (APP). METHODOLOGY/PRINCIPAL
findingsLactic acid increased levels of Aβ40 and 42, as measured by ELISA, in culture medium of human neuroblastoma cells (SH-SY5Y), whereas it decreased APP metabolites, such as sAPPα. In cell lysates, APP levels were increased and APP was found to interact with ER-chaperones in a perinuclear region, as determined by co-immunoprecipitation and fluorescence microscopy studies. Lactic acid had only a very modest effect on cellular pH, did increase the levels of ER chaperones Grp78 and Grp94 and led to APP aggregate formation reminiscent of aggresomes. CONCLUSIONS/SIGNIFICANCE: These findings suggest that sustained elevations in lactic acid levels could be a risk factor in amyloidogenesis related to Alzheimer's disease through enhanced APP interaction with ER chaperone proteins and aberrant APP processing leading to increased generation of amyloid peptides and APP aggregates.
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Registered trials
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