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Aging (Aging-US) Research

Aging-US Research

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Aging (Aging-US) Research

Figure 7. Schematic illustration of the lipodystrophy and insulin resistance exhibited by patients with Werner syndrome.
Aging Blog News

Rapamycin’s Therapeutic Potential in Treating Werner Syndrome

October 26, 2023October 26, 2023

In this new study, researchers from Japan investigated the molecular mechanisms of subcutaneous fat dysfunction in Werner syndrome.

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Dr. Mikhail Blagosklonny interview
Aging Misha Blagosklonny News Spotlight

Dr. Mikhail Blagosklonny on Rapamycin Longevity Series

September 7, 2023September 7, 2023

Dr. Mikhail Blagosklonny joins “Master One Thing” host Krister Kauppi to discuss the impact of his rapamycin research and hyperfunciton theory of aging.

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Late-in-Life Interventions to Improve Cardiac Health
Aging Blog News

Late-in-Life Interventions to Improve Cardiac Health

December 28, 2022January 3, 2023

In a new research perspective, researchers discuss spermidine, rapamycin, caloric restriction, and exercise training to improve cardiac health in aging individuals.

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Hallmarks of Cancer and Aging
Aging Blog News

An Original Review on the Hallmarks of Cancer and Aging

May 19, 2022May 20, 2022

Dr. Mikhail Blagosklonny published an original review paper in Aging (Aging-US) Volume 14, Issue 9, entitled, “Hallmarks of cancer and hallmarks of aging.”

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Altos Labs
Aging Blog News

Dr. Blagosklonny’s Rapamycin-Based Recommendation for Altos Labs

May 12, 2022May 18, 2022

Mikhail Blagosklonny, M.D., Ph.D., has a recommendation for Altos Labs in his new research perspective, entitled, “Altos Labs and the quest for immortality: but can we live longer right now?”

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Figure 16. Influences of mutant and WT-TP53 on mitochondrial activity and glucose metabolism and effects of rapamycin and metformin. The effects of WT and mutant TP53 on key enzymes important in glycolysis and how they can influence metabolism and PDAC tumor growth. In our studies, we have examined the effect of GOF mutant TP53 and in some cases WT TP53. In addition, sites of interaction of the type 2 diabetes drug metformin and the immunosuppressive drug rapamycin and their effects on AMPK and mTORC1 are indicated. TP53 can induce mitochondrial apoptosis pathway by regulating the expression of PUMA and other proteins.
Aging Blog News

TP53 Restoration Sensitizes Pancreatic Cancer to Multiple Drugs

May 4, 2022May 30, 2022

In Aging’s Volume 14, Issue 8, cover paper, researchers found that the restoration of wild-type TP53 decreased pancreatic cancer cell resistance to various drugs, including rapamycin.

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Radiation therapy, advanced medical linear accelerator in therapeutic oncology to treat cancer
Aging News Trending

Trending With Impact: Radiation, Senescence and Senotherapeutics

February 18, 2022February 20, 2022

Researchers investigated radiation-induced senescent cells and their effects on tumor growth, and senotherapeutics to mitigate these effects.

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Figure 1. Relationship between aging and diseases. When growth is completed, growth-promoting pathways increase cellular and systemic functions and thus drive aging. This is a pre-pre-disease stage, slowly progressing to a pre-disease stage. Eventually, alterations reach clinical disease definition, associated with organ damage, loss of functions (functional decline), rapid deterioration and death.
Aging News

Aging Is Easily Treatable

July 13, 2021February 4, 2022

In 2018, Dr. Mikhail Blagosklonny wrote a thought provoking theory article, entitled: “Disease or not, aging is easily treatable.”

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Aging News

Rapamycin: The Miracle Compound From Easter Island

July 8, 2021February 4, 2022

What was found buried in the dirt on Easter Island in 1964 was a compound that would mystify aging researchers for the next 50 years.

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Aging News

Complex Drug Screenings Show Anti-Aging Potential in Natural Compounds

May 5, 2021February 4, 2022

In an effort to mimic metformin and rapamycin, researchers used powerful screening methods to analyze over 800 natural compounds to assess their anti-aging potential and safety profile.

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