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TA-65 administration during 4 months significantly improved the capacity to uptake glucose after a glucose pulse

liver protective action of TA-65

A disadvantage of mTERT potentiation could be associated to its capacity to favor proliferation of cancerous cells in murine models

TA-65 treated mice presented a similar incidence of malignant cancers at time of death, with a tendency to show decreased sarcomas and slightly increased lymphomas

We demonstrate here that TA-65 leads to a significant rescue of short telomeres through telomerase activation

TA-65 treatment increases proliferation and mobilization potential of mouse keratinocytes in vitro, a situation mimicking telomerase overexpression

TAT2, a similar molecule, have beneficial effects in the activation of CD8+ T lymphocytes from HIV-infected patients where they observe an increase of the proliferative potential and enhancement of cytokine/chemokine production

TA-65 resulted in a similar rescue of short telomeres in leukocytes post-treatment as observed with humans, most likely through an activation of telomerase

we observe that TA-65 lead to 10 fold increase of telomerase RNA levels in the liver of treated mice comparing to the non-treated same-age cohorts

TA-65 regulates telomerase at the transcription level, probably through the regulation of the MAPK pathway

TA-65 dependent telomerase activation results in a better organ fitness as demonstrated by the improved scores at the glucose tolerance test and insulin levels at fasting

TA-65 supplemented mice also present modest enhancement of the subcutaneous and epidermal thickness, as well as higher bone density, representative of an overall fitness status improvemen

TA-65 treated mice present higher levels of RBC and hemoglobin comparing to the control cohorts

improved health-span of TA-65 treated mice is not accompanied by increased cancer incidence, which may be related to the fact that TERT levels are very modestly increased in all tissues tested except for the liver

systemic telomerase overexpression from the germline leads to protection from aging associated pathologies

similar situation could be mimicked expressing telomerase late in life in a telomerase deficient background

we observed a higher proliferation rate and a partial protection from cell death in some tissues of TA65 treated mice