Language
Bilal Bawamiya, Luke Spray, Vincent K. Wangsaputra, Karim Bennacer, Shalalai Wahabi, Constantinos Stross, Ehsan Haratikupay, Emmanuel Ogondimou, Chris P. Gale, Bernard Kefney, Rebecca Mayer, Helen H.

Bilal Bawamia, Luke Spree, Vincent King Saputra, Karim Benaser, Salareh Wahhabi, Constantinus Stelros, Ahsan Haratikupai, Emmanuel Ogundim, Chris Gael, Bernard Cavani, Rebecca Mayer, Helen Hancock, Gavin Richardson, David Austin, Joachim Spiridoplos


Geographic Science (2023)


Background


Myocardial infarction (MI) or heart attack is a major disease that increases the risk of cardiovascular recurrence or death. One factor leading to these adverse consequences is premature aging of the immune system, also known as "immune aging". Recent research has focused on the role of TA-65 (an oral telomerase activator) and its potential to counteract immune cell aging in patients after myocardial infarction. Previous studies and preclinical data have shown that TA-65 can reduce immune system aging and inflammation after myocardial infarction.


Research Model


This tactical trial is a single center, randomized, double-blind, parallel group, placebo-controlled 2A trial study involving 90 participants diagnosed with coronary heart disease and myocardial infarction within the past 6 months. Participants received a dose of 8 milligrams of TA-65 or placebo twice a day for 12 months. This trial is mainly aimed at patients aged 65 and above who have suffered from acute myocardial infarction within the past 6 months and have successfully undergone vascular reconstruction or received medication treatment after myocardial infarction. Exclude patients with immune dysfunction, clinical instability, severe uncontrolled hypertension, serious comorbidities or other special circumstances that may affect outcomes in the next two years.


This experiment used multiple detection methods to track the response to TA-65 treatment, including flow cytometry analysis of white blood cells, quantification of nuclear telomerase activity in peripheral blood mononuclear cells (PBMCs) using telomerase repeat activation protocol (TRAP) - quantitative polymerase chain reaction (qPCR) detection, and evaluation of oxidative stress using TBARS colorimetric assay.


Survey results and action methods


The experimental results showed that after 12 months, TA-65 treatment resulted in a significant increase in the average total lymphocyte count. This increase is mainly due to a significant increase in CD3+, CD4+, and CD8+T lymphocytes, B lymphocytes, and natural killer cells compared to baseline. No such increase was observed in the placebo group. In addition, after 12 months, the inflammation marker hsCRP in the TA-65 group decreased by 62% compared to the placebo group. Importantly, the TA-65 group also experienced significantly fewer complications after a heart attack, such as chest or joint pain.


From the perspective of mechanism of action, activation of mitochondrial telomerase is a potential pathway for TA-65 to exert its effects. Activation of telomerase within mitochondria can improve their function, contributing to overall cellular health and vitality. This is particularly helpful for the regeneration of T cells, which often experience mitochondrial dysfunction, leading to aging and inflammation - a chronic inflammatory state associated with aging.


Survey results, health impact


The tactical test results showed that TA-65 could enhance the health of immune cells, reduce inflammation, potentially delay the progress of coronary atherosclerosis, and reduce the incidence of heart failure in patients with myocardial infarction. This experiment shows that TA-65 can not only reduce inflammation, but also enhance immunity by increasing the patient's immune cells.


Survey results, safety


TA-65 demonstrated good safety, with a significant reduction in observed adverse events compared to the placebo group. The TA-65 group rarely experienced adverse reactions after a heart attack, such as fever or new medical problems, and reduced adverse reactions by 30% compared to the placebo group. This positive safety feature, combined with observed health benefits, suggests that TA-65 can serve as a promising new treatment for patients after myocardial infarction.


Conclusion


The findings of tactical experiments emphasize the potential of TA-65 in combating immune aging and enhancing immune function, especially in individuals after MI. TA-65 is known for its significant ability to inhibit inflammation, reducing inflammation by up to 62%, while enhancing immunity by increasing the number of immune cells. Considering that many potent anti-inflammatory drugs often suppress the immune system, this dual effect is indeed worth noting. In addition, its good safety makes TA-65 a convincing treatment option for managing common residual issues of immune aging after myocardial infarction.


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By visiting the complete research, gain a deeper understanding of the comprehensive details of our breakthrough research: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10122201/