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Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice.
Brain Res. 2008 Jun 12; 1214:177-87.BR

Abstract

We previously reported that intraperitoneal (i.p.) injection (20 mg/kg) of (-)-epigallocatechin-3-gallate (EGCG), the main polyphenolic constituent of green tea, decreased beta-amyloid (Abeta) levels and plaques via promotion of the non-amyloidogenic alpha-secretase proteolytic pathway in "Swedish" mutant amyloid precursor protein overexpressing (APPsw, Tg) mice. Here, we find that EGCG administered orally in drinking water (50 mg/kg) similarly reduces Abeta deposition in these mice. Following a six month treatment of an 8 month old cohort, immunohistochemical analysis of coronal sections reveals that plaque burdens were reduced in the cingulate cortex, hippocampus, and entorhinal cortex by 54%, 43%, and 51%, respectively. Congo red plaque burdens were decreased in the cingulate cortex, hippocampus, and entorhinal cortex by 53%, 53%, and 58%, respectively as well. ELISA of brain homogenates of the treatment Tg mice revealed consistent reductions in both Abeta1-40 and 1-42 soluble and insoluble forms. In the present study we also investigated the effect EGCG administration had on tau pathology and cognition in Tg mice. Both i.p. and orally-treated Tg animals were found to have modulated tau profiles, with markedly suppressed sarkosyl-soluble phosphorylated tau isoforms. Radial arm water maze (RAWM) testing for working memory indicated that EGCG provided cognitive benefit to Tg mice with both i.p. and oral administration, although i.p.-treated animals showed a more pronounced benefit because of the greater impairment of their Tg controls at the time of testing. Taken together, these data further the notion of EGCG dietary supplementation as a potentially safe and effective prophylaxis for Alzheimer's disease.

Authors+Show Affiliations

Rashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Department of Psychiatry and Behavioral Medicine, and Department of Neurosurgery, University of South Florida, Tampa, FL 33613, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

18457818

Citation

Rezai-Zadeh, Kavon, et al. "Green Tea Epigallocatechin-3-gallate (EGCG) Reduces Beta-amyloid Mediated Cognitive Impairment and Modulates Tau Pathology in Alzheimer Transgenic Mice." Brain Research, vol. 1214, 2008, pp. 177-87.
Rezai-Zadeh K, Arendash GW, Hou H, et al. Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice. Brain Res. 2008;1214:177-87.
Rezai-Zadeh, K., Arendash, G. W., Hou, H., Fernandez, F., Jensen, M., Runfeldt, M., Shytle, R. D., & Tan, J. (2008). Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice. Brain Research, 1214, 177-87. https://doi.org/10.1016/j.brainres.2008.02.107
Rezai-Zadeh K, et al. Green Tea Epigallocatechin-3-gallate (EGCG) Reduces Beta-amyloid Mediated Cognitive Impairment and Modulates Tau Pathology in Alzheimer Transgenic Mice. Brain Res. 2008 Jun 12;1214:177-87. PubMed PMID: 18457818.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice. AU - Rezai-Zadeh,Kavon, AU - Arendash,Gary W, AU - Hou,Huayan, AU - Fernandez,Frank, AU - Jensen,Maren, AU - Runfeldt,Melissa, AU - Shytle,R Douglas, AU - Tan,Jun, Y1 - 2008/04/07/ PY - 2007/12/06/received PY - 2008/02/07/revised PY - 2008/02/10/accepted PY - 2008/5/7/pubmed PY - 2008/9/20/medline PY - 2008/5/7/entrez SP - 177 EP - 87 JF - Brain research JO - Brain Res VL - 1214 N2 - We previously reported that intraperitoneal (i.p.) injection (20 mg/kg) of (-)-epigallocatechin-3-gallate (EGCG), the main polyphenolic constituent of green tea, decreased beta-amyloid (Abeta) levels and plaques via promotion of the non-amyloidogenic alpha-secretase proteolytic pathway in "Swedish" mutant amyloid precursor protein overexpressing (APPsw, Tg) mice. Here, we find that EGCG administered orally in drinking water (50 mg/kg) similarly reduces Abeta deposition in these mice. Following a six month treatment of an 8 month old cohort, immunohistochemical analysis of coronal sections reveals that plaque burdens were reduced in the cingulate cortex, hippocampus, and entorhinal cortex by 54%, 43%, and 51%, respectively. Congo red plaque burdens were decreased in the cingulate cortex, hippocampus, and entorhinal cortex by 53%, 53%, and 58%, respectively as well. ELISA of brain homogenates of the treatment Tg mice revealed consistent reductions in both Abeta1-40 and 1-42 soluble and insoluble forms. In the present study we also investigated the effect EGCG administration had on tau pathology and cognition in Tg mice. Both i.p. and orally-treated Tg animals were found to have modulated tau profiles, with markedly suppressed sarkosyl-soluble phosphorylated tau isoforms. Radial arm water maze (RAWM) testing for working memory indicated that EGCG provided cognitive benefit to Tg mice with both i.p. and oral administration, although i.p.-treated animals showed a more pronounced benefit because of the greater impairment of their Tg controls at the time of testing. Taken together, these data further the notion of EGCG dietary supplementation as a potentially safe and effective prophylaxis for Alzheimer's disease. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/18457818/Green_tea_epigallocatechin_3_gallate__EGCG__reduces_beta_amyloid_mediated_cognitive_impairment_and_modulates_tau_pathology_in_Alzheimer_transgenic_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(08)00409-5 DB - PRIME DP - Unbound Medicine ER -