Aging inevitably increases the risk of disease, as exemplified by CAD, AD, and cancer. Monitoring the aging process and understanding its mechanisms will not only enhance early diagnoses, it may also provide strategies for the early prevention and treatment of diseases. While biomarkers for cellular senescence in in vitro cultured mammalian cells are already well-defined, those that define in vivo senescence/aging at the systemic level remain scarce. Here, we generated a targeted Glb1^+/m allele at the Glb1 locus that encodes β-galactosidase. The GAC signal indicates Glb1 level. The results reveal that the live-imaged GAC signal is linearly correlated with chronological age, but only in middle-aged mice (9–13 months). High GAC at the MA stage was associated with cardiac hypertrophy and shortened lifespan. Moreover, GAC signal was exponentially increased in pathological lung fibrosis induced by BLM. Thus, this in vivo reporter mouse can faithfully monitor systemic aging and organ functional decline in a manner closely associated with lifespan, and provides an ideal system for studying aging mechanisms and developing anti-aging manipulations.

The upregulation of p16^Ink4a transcription and elevated SAβ-gal staining are both well-established and widely used biomarkers for cellular senescence¹⁷, and the former led to the generation of live-imaging aging reporter mice^20,22,23. Intriguingly, high level of p16^Ink4a, indicated by luciferase activity, predicts cancer initiation rather than lifespan. Similarly, the in vivo application of SAβ-gal as a senescence marker at the tissue level is also limited. Positive SAβ-gal-staining is easy to obtain in kidney and adipose tissue sections but difficult to obtain in blood vessel and heart sections. By SAβ-gal staining, not many positive cells were detected in old individuals²⁶. It raises the question of whether SAβ-gal labels in vivo senescence or if the percentage of in vivo senescent cells is indeed very low.

New advances in medical science may improve health of older people and extend lift, perhaps just long enough for more advanced future therapies.#longevity #health #healthspan What is the next step and how can we combine different therapies and test if we can rejuvenate an adult mouse, and humans?Our guest speaker Aubrey de Grey present what may come next.

If you wish to check the links to the sites mentioned in the discussion: https://www.levf.orghealthspanaction.orga4li.orglessdeath.orgTo donate to Longevity Escape Velocity Foundation (LEVF) and to the rejuvenation research:

https://www.levf.org/

Age-related macular degeneration (AMD) is the most common cause of vision loss among people aged 50 and older, affecting an estimated 7.3 million individuals in the United States. Of these patients, 1.75 million have advanced AMD and will lose vision from this condition. This includes patients with the “wet” form of AMD, characterized by the growth of abnormal blood vessels in the retina that can bleed or leak damaging fluids into the central portion of this light-sensing tissue.

“Our goal is to re-regulate all of your genes back to an earlier state.” Excellent. Hurry please. I’m 51.

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In this video Dr Davidsohn discusses the next generation therapies that Rejuvenate Bio are working on. We also discuss, klotho, RJB02 and his personal protocol.

One of the world’s leading hospitals is preparing to offer longevity clinical services to patients. Sheba Medical Center in Tel Aviv, Israel, is poised to open a dedicated longevity centre in 2023, with the goal of democratising the extension of healthy lifespan for the masses.

Longevity. Technology: While research, development and investment in longevity are at an all-time high, the implementation of longevity clinical practice in mainstream healthcare is virtually non-existent. While private clinical practices are now making longevity services accessible to those who can afford it, the societal benefit of improving healthspan can only be realised if everyone can access it. To learn more, we caught up with Professor Tzipi Strauss, Director of Neonatology at Sheba Hospital, who is the driving force behind the new centre.

It may seem curious that a paediatrician is the instigator of an initiative focused on improving aging, but Strauss explains that the relevance of longevity begins at birth.

Cardiac alterations in structure and function, namely, the left ventricle, have been intensely studied for decades, in association with aging. In recent times, there has been keen interest in describing myocardial changes that accompany skeletal muscle changes in older adults. Initially described as a cardio-sarcopenia syndrome where alterations in myocardial structure were observed particularly among older adults with skeletal muscle sarcopenia, investigations into this syndrome have spurred a fresh level of interest in the cardiac-skeletal muscle axis. The purpose of this perspective is to summarize the background for this “syndrome of concern,” review the body of work generated by various human aging cohorts, and to explore future directions and opportunities for understanding this syndrome.

The traditional view of cardiovascular aging is that of age-related adaptations in the heart characterized by increased left ventricular (LV) mass (LVM) and LV hypertrophy (LVH), which are often secondary to increased systolic blood pressure mainly mediated by arterial stiffening (1, 2). These changes accumulate throughout the lifetime of an individual, increasing the risk of developing cardiovascular disease (CVD), such as heart failure (HF) and coronary artery disease. The incidence of CVD increases with age, rising from ∼78% among adults aged 60–79 years to ∼90% in those aged above 80 years. CVD is the leading cause of disease burden in the world, with global prevalence doubling from 271 million to 523 million between 1990 and 2019. Incident CVD mortality increased from 12.1 million to 18.6 million in the same period , and accounted for 32% of all deaths. With rapidly aging national populations, these numbers are expected to increase.