Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice.
Level 5 - mechanism / opinion, no new human data
Preclinical animal study in transgenic mice
PubMed 18457818 · doi:10.1016/j.brainres.2008.02.107
What was done
Swedish mutant amyloid precursor protein overexpressing (APPsw, Tg) mice (8-month-old cohort) were treated for 6 months with green tea epigallocatechin-3-gallate (EGCG) orally in drinking water (50 mg/kg) or via intraperitoneal (i.p.) injection. The researchers evaluated beta-amyloid (Abeta) plaque burdens in coronal sections of the cingulate cortex, hippocampus, and entorhinal cortex using immunohistochemistry and Congo red staining, measured soluble and insoluble Abeta1-40 and 1-42 levels by brain homogenate ELISA, analyzed sarkosyl-soluble phosphorylated tau isoforms, and assessed working memory via the radial arm water maze (RAWM).
What was found
Oral EGCG reduced immunohistochemical plaque burden in the cingulate cortex by 54%, hippocampus by 43%, and entorhinal cortex by 51%. Congo red plaque burdens decreased by 53% in the cingulate cortex, 53% in the hippocampus, and 58% in the entorhinal cortex. ELISA showed reductions in both soluble and insoluble Abeta1-40 and 1-42 forms. Both oral and i.p. treatment markedly suppressed sarkosyl-soluble phosphorylated tau isoforms and improved working memory on RAWM testing.
Why it matters
The findings indicate that oral administration of the green tea polyphenol EGCG can reduce both amyloid and tau pathologies and mitigate cognitive deficits in an Alzheimer's disease mouse model.
Limits
The study is limited to transgenic mice and does not provide human clinical or pharmacokinetic data. The abstract does not report the total sample size (n), variance metrics, or exact p-values.
Cited by
- partial Green tea extract and blueberry extract have been demonstrated to decrease beta-amyloid plaques.