As we age, our immune system ages with us. Thankfully, there are ways to slow or even reverse the aging of the immune system.
References and additional information:
The immune system eliminates pre-cancer cells daily ([ Ссылка ]), it is involved in the development of heart diseases ([ Ссылка ]), and even Alzheimer’s is, at least in some cases, driven by inflammation ([ Ссылка ]).
Vaccinations work less well in the elderly ([ Ссылка ]) and old people are more likely to die from infectious diseases ([ Ссылка ] and [ Ссылка ])
Rapamycin extends the lifespan of mice ([ Ссылка ]), fruits flies ([ Ссылка ]) and worms ([ Ссылка ]) and is currently tested in dogs.
The three changes during immunosenescence are nicely described here: [ Ссылка ]
Chen et al. showed that mTOR becomes more active during aging and using genetically modified animals they could speed up the aging process of hematopoietic stem cells (HSC; immune system stem cells) by continuous mTOR activation. Using rapamycin to block mTOR activation, the researchers showed an increase in HSC proliferation in old animals. The increase in HSC leads to an increase in B cell progenitors and B cells (important cells for vaccine efficiency) and a decrease in macrophages (cells of the innate immune system). This reversal in ‘immunosenescence’ was associated with improved vaccine efficiency in old animals. Instead of 70% of old but vaccinated animals dying, none of the animals died!
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Mannick et al. followed up on the findings and performed a clinical trial giving elderly volunteers three different regiments of RAD001 (a rapamycin analog that also inhibits mTOR). The doses were: 0.5 mg daily, 5 mg weekly, or 20 mg weekly. The subjects were treated for 6 weeks with the study drug and, after a 2-week drug-free interval, were given a 2012 seasonal influenza vaccine. The antibody titer to influenza vaccine strains was increased in the treatment groups compared to the placebo and ti also reduced the percentage of CD4 and CD8 T lymphocytes expressing the programmed death-1 (PD-1) receptor, which inhibits T cell signaling and is more highly expressed with age. [ Ссылка ]
Cheng (2014) and Brandhorst (2015) et al showed that prolonged fasting and fasting-mimicking diets (FMD) lead to similar effects seen with rapamycin treatment. In both cases, they saw increased HSC renewal and a shift towards more lymphoid cells. They also found that the FMD reversed age effects in other tissues, such as the muscles and bones in animals. Finally, using the FMD in humans reduces C-reactive protein levels in subjects that had high CRP levels at baseline.
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Chronic inflammation is associated with aging ([ Ссылка ]), likely drives aging ([ Ссылка ] ) and age-related diseases ([ Ссылка ] and [ Ссылка ])
