Lifeboat Foundation

The writer is the author of “Extra Time: Ten Lessons for an Ageing World”

Is the rash of US presidential candidates aged over 70 a sign of weakness or strength? We hear that Bernie Sanders isn’t too left; he’s too old. Michael Bloomberg was alive when Harry Truman was in the White House. Joe Biden is surely as worn out as his shoe leather.

In reality, all of these characters seem in remarkably good shape. Despite being the oldest president ever to be sworn in (he was 69), Donald Trump still acts like a kid.

Researchers report an advance in the development of a blood test that could help detect pathological Alzheimer’s disease in people who are showing signs of dementia. This approach could be less invasive and less costly than current brain imaging and spinal fluid tests. The blood test detects the abnormal accumulation of a form of tau protein known as phosphorylated-tau-181 (ptau181), which is a biomarker that suggests brain changes from Alzheimer’s. The study, funded by the National Institutes of Health, was published on March 2 in Nature Medicine.

Over the past 15 years, research advances in the development of biomarkers like tau protein have enabled investigators to more accurately diagnose Alzheimer’s disease, select research participants, and measure response to investigational therapies. Tau and other biomarkers can be detected with PET scans of the brain and lab tests of spinal fluid. However, PET imaging is expensive and involves radioactive agents, and spinal fluid tests require spinal taps, which are invasive, complex and time-consuming. Simpler biomarker tests are still needed.

“The considerable time and resources required for screening research participants with PET scans and spinal taps slow the pace of enrollment for Alzheimer’s disease treatment studies,” said Richard J. Hodes, M.D., director of NIH’s National Institute on Aging (NIA), which funded much of the study. “The development of a blood test would enable us to rapidly screen a much larger and more diverse group of volunteers who wish to enroll in studies.”

1️⃣ Genomic Instability 2️⃣ Telomere Attrition 3️⃣ Epigenetic Alterations 4️⃣ Loss of Proteostasis 5️⃣ Nutrient Sensing Goes Awry 6️⃣ Mitochondrial Dysfunction 7️⃣ Cellular Senescence 8️⃣ Stem Cell Exhaustion 9️⃣ Altered Intercellular Communication.

Explore these horsemen and the strategies being deployed to defeat this decline in Chapter 10 — The Future of #Longevity ➡️ futurefasterbook.com

However, labeling aging itself as a disease is both misleading and detrimental. Pathologizing a universal process makes it seem toxic. In our youth-obsessed society, ageism already runs rampant in Hollywood, the job market, and even presidential races. And calling aging a disease doesn’t address critical questions about why we age in the first place. Instead of calling aging a disease, scientists should aim to identify and treat the underlying processes that cause aging and age-related cellular deterioration.

Aging is associated with heart disease, Alzheimer’s, diabetes, and cancer, but what’s underlying all that?

the photo series by vintner and fletcher illustrates three gradual stages of transhumanism from ‘testing ground’, ‘patient zero’ to ‘humanity 2.0’. at the lowest tier, ‘testing ground’ looks into individuals who have created wearable technology to expand their human abilities, improving everything from concentration to mental health.‘patient zero’ studies those who have taken permanent action to become half human and half robot. in the final chapter, ‘humanity 2.0’, the transhumanist subjects focus on life extension and immortality.

I think so.

A handful of clinical trials are underway to find out whether drugs that target senescent cells can slow the ravages of old age.

Yet another talk from Aubrey.

Are you the one?

THE FIRST human to live for over 1,000 years is probably already alive according to Dr Aubrey de Grey, a British scientist who is working to stop human ageing.

I think I can speak for us older folks on this…YAY!

AgeX converts the cells of deceased 114-year-old into young pluripotent stem cells; evidence of telomere aging reversal in a supercentenarian’s cells.