Component

Entorhinal cortex

Entorhinal cortex. Species, exposure and limitations are retained in each linked claim.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

Where it participates (unsigned role)

  1. In APPsw transgenic mice, ibuprofen effects were not mediated by alterations in amyloid precursor protein expression or oxidative damage, six months of treatment in transgene-positive females decreased open field behaviour to values similar to transgene-negative mice and reduced caspase activation per plaque, and a shorter three month trial begun at 14 months produced a significant treatment effect on amyloid-beta levels with reductions of both soluble amyloid-beta and amyloid-beta 42 most marked in entorhinal cortex, the magnitude of the effect on soluble amyloid-beta not depending on treatment duration.

    Ibuprofen → Amyloid-beta 42, the 42-residue isoform source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/ibuprofen-research/11755007.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85bd65aa6bff20262f11cfa0cd26a25a327aff114898605cea3a0cc05459192b", "start_char": 0, "end_char": 1213, "text_sha256": "85bd65aa6bff20262f11cfa0cd26a25a327aff114898605cea3a0cc05459192b"}
    experimental_model
    Six month and three month ibuprofen treatment of APPsw Tg2576 transgenic mice with behavioural and biochemical endpoints
    exposure
    Ibuprofen begun at different ages, with soluble and insoluble amyloid-beta and open field behaviour measured
    limitations
    An in vivo test with a behavioural endpoint and two treatment durations. A transgenic model of amyloid deposition, which is not Alzheimer’s disease.
    nutrient_topic
    Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. · Ibuprofen
    organism
    Mouse
    plain_language
    In mice bred to deposit amyloid, the drug lowered the peptide and changed their behaviour back toward normal.
    primary_references
    [ibu-p11755007] Ibuprofen effects on Alzheimer pathology and open field activity in APPsw transgenic mice. (2001). https://pubmed.ncbi.nlm.nih.gov/11755007/ DOI: 10.1016/s0197-4580(01)00299-8
    tissue_or_cell_type
    Brain

    Ibuprofen: the enantiomer that works, the one that was called inactive, the one-way chemistry that turns one into the other, and the targets that are not cyclooxygenase (2026-09-22) · lines 435–446

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six month and three month ibuprofen treatment of APPsw Tg2576 transgenic mice with behavioural and biochemical endpoints · source_derived_draft · unverified_draft

    ### ibu-in-vivo-and-behavioural In APPsw transgenic mice, ibuprofen effects were not mediated by alterations in amyloid precursor protein expression or oxidative damage, six months of treatment in transgene-positive females decreased open field behaviour to values similar to transgene-negative mice and reduced caspase activation per plaque, and a shorter three month trial begun at 14 months produced a significant treatment effect on amyloid-beta levels with reductions of both soluble amyloid-beta and amyloid-beta 42 most marked in entorhinal cortex, the magnitude of the effect on soluble amyloid-beta not depending on treatment duration. Condition category: normal nutrient_topic: Ibuprofen research collection; topical membership is not evidence of a direct clinical effect, and the racemate is recorded separately from each of its two enantiomers. plain_language: In mice bred to deposit amyloid, the drug lowered the peptide and changed their behaviour back toward normal. organism: Mouse tissue_or_cell_type: Brain experimental_model: Six month and three month ibuprofen treatment of APPsw Tg2576 transgenic mice with behavioural and biochemical endpoints limitations: An in vivo test with a behavioural endpoint and two treatment durations. A transgenic model of amyloid deposition, which is not Alzheimer’s disease. exposure: Ibuprofen begun at different ages, with soluble and insoluble amyloid-beta and open field behaviour measured evidence_span: {"source_cache": "artifacts/ibuprofen-research/11755007.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "85bd65aa6bff20262f11cfa0cd26a25a327aff114898605cea3a0cc05459192b", "start_char": 0, "end_char": 1213, "text_sha256": "85bd65aa6bff20262f11cfa0cd26a25a327aff114898605cea3a0cc05459192b"} [ibu-p11755007] Ibuprofen effects on Alzheimer pathology and open field activity in APPsw transgenic mice. (2001). https://pubmed.ncbi.nlm.nih.gov/11755007/ DOI: 10.1016/s0197-4580(01)00299-8
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards