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Keywords:

  • Alzheimer's disease;
  • Aβ-derived diffusible neurotoxin ligands;
  • cell cultures;
  • flavanols;
  • rat hippocampus

Abstract

Teas represent a large family of plants containing high amounts of polyphenols that may confer health benefits in various diseases. Recently, it has been hypothesized that tea consumption may also reduce the risk of age-related neurodegenerative pathologies. Considering the deleterious role of β-amyloid (Aβ) in the aetiology of Alzheimer's disease (AD), we investigated green and black tea extracts and flavan-3-ols (present as monomers and dimers in green and black forms, respectively) against toxicity induced by Aβ-derived peptides using primary cultures of rat hippocampal cells as model. Both green and black tea extracts (5–25 µg/mL) displayed neuroprotective action against Aβ toxicity. These effects were shared by gallic acid (1–20 µm), epicatechin gallate (ECG; 1–20 µm) and epigallocatechin gallate (EGCG; 1–10 µm), the former being the most potent flavan-3-ol. In contrast, epicatechin and epigallocatechin were ineffective in the same range of concentrations. Moreover, only tea flavan-3-ol gallate esters (i.e. ECG, EGCG) and gallic acid inhibited apoptotic events induced by Aβ25-35. Interestingly, EGCG and gallic acid inhibited Aβ aggregation and/or the formation of Aβ-derived diffusible neurotoxin ligands. Taken together, these results indicate that the catechin gallates (through the galloyl moiety) contribute to the neuroprotective effects of both green and black teas. Moreover, the protective effect of EGCG is likely to be associated, at least in part, with its inhibitory action on Aβ fibrils/oligomers formation. These data also support the hypothesis that not only green but also black teas may reduce age-related neurodegenerative diseases, such as AD.