We explore the essence of aging to develop theories of pinpoint precision. Unlike traditional disease-oriented research, our work starts from the foundational TRCS model to uncover the most fundamental biological mechanisms, aiming to establish the scientific groundwork for significant lifespan extension.
To develop life-extending methods, we must first identify the cause and biochemical mechanism of aging, and subsequently design solutions based on this cause and mechanism.
Aging is an extremely complex systemic issue. If we disregard its fundamental causal mechanisms and rely solely on chance discoveries in the laboratory, it would be tantamount to shooting in the dark, with minimal probability of success. Therefore, we can state that money, laboratories, and technicians alone cannot achieve rejuvenation; we must first have the correct theory. This is the fundamental reason we focus on theoretical research.
Currently, there are over 300 aging hypotheses in the scientific community, with almost every hypothese giving rise to corresponding anti-aging methods. However, the vast majority of these hypotheses may be incorrect—which also explains why no method has yet succeeded in truly reversing human aging or significantly extending lifespan.
Our mission is to eliminate erroneous hypotheses and methods through rigorous logical reasoning, enabling the field to avoid detours and unnecessary resource waste—after all, our time and funding are precious and cannot be expended without constraint.
For advanced challenges like aging, theoretical capability is more important than practical ability. Correct theory can provide answers and guide research direction. Just as Einstein, who was unskilled with his hands, could theorize about gravitational waves—and later generations found evidence based on his theory.
Our institute focuses on the study of biological aging mechanisms and, based on this foundation, explores innovative pathological mechanisms and therapeutic strategies for major age-related diseases such as neurodegenerative diseases and cancer.
A concise overview of the TRCS model's core principles.
Bilu Huang's TRCS aging model shows that aging is essentially a genetic program driven by telomeres and/or rDNA shortening through the p53 pathway, rather than the accumulation of damage. Individual aging results from replicative senescence of adult stem cells; and that cellular senescence is co-regulated by telomeres and rDNA through the p53 pathway. Moreover, the 11 other classic hallmarks of aging are downstream events regulated by p53 upregulation after telomere and rDNA shortening. From the perspective of first principles, the lifespan of a species is determined by the shortening rate of telomeres and rDNA arrays.
The acronym TRCS represents four interconnected pillars:
The classic cause of replicative senescence and the Hayflick limit.
Plays a more significant role than telomeres in driving cellular senescence.
It's not one countdown timer, but two interconnected systems.
The state where cells experience functional decline and alteration during aging.
Content to be developed. This section will detail Bilu Huang's new pathological mechanisms and treatment strategies for neurodegenerative diseases, based on the TRCS model.
Content to be developed. This section will detail Bilu Huang's new pathological mechanisms and treatment strategies for cancer, based on the TRCS model.
Bilu Huang has conducted a systematic and in-depth critique of prevailing aging theories and anti-aging methodologies.
Read the Full Critical Analysis