Everything we do comes with a cost. So does everything we don't do.

This isn't a Yogi Berra quote. It's just one way to explain opportunity cost.

Failing to act can be expensive. No, we're not talking about that stamp you didn't buy thirty years ago.

We're talking more about brushing daily to avoid the expense (and pain) of a root canal. After all, costs aren't always monetary. This is why we're so enthusiastic about gene therapy: besides proving itself on a variety of monogenic diseases, it shows tremendous promise in keeping complex issues, like cognitive decline, from taking root.

That's why BioViva is now building on the success of a human dementia study. We analyzed its exciting results in 2021.

Subjects received hTERT (to lengthen telomeres) and Klotho. Published in the Journal of Regenerative Medicine and Biology, its success added even more credibility to BioViva's vision for regenerative medicine.

We invite you to share and support what will surely be another landmark event in longevity research. Almost all of us know someone, or care about someone, with a neurodegenerative disease. Many of us, if we live long enough, will develop one. BioViva wants to make Alzheimer's and its ilk things of the past.

For over a hundred years she has sat 12,600 feet underwater.

A person who is struck by lightning in a drizzle is worthy of our sympathy. It's just bad luck. Other unfortunates are more than unlucky.

Edward Smith, captain of the RMS Titanic, was warned six times about icebergs. While the last and most dire of these allegedly never made it to his desk, it is still hard to give him a pass (Smith canceled the scheduled lifeboat drill on the day of the collision).

To make matters worse, the ship, which could hold 64 lifeboats, was only outfitted with 20. White Star Lines felt more would detract from the deck's decor.

Besides, why would a “practically unsinkable” vessel need them?

Mistakes have a way of piling up when everyone accepts a faulty premise. Among the faultiest is believing we can treat disease without addressing the aging process. Remember, our bodies have no backups. There are no lifeboats for the chronically ill, and aging is undeniably the world's deadliest disease.

Hollywood's romanticization aside, the Titanic is only a story of hubris at first glance.

There were commentators, and even passengers, who were pessimistic about its maiden voyage. They thought the rush to build bigger and faster boats was bound to end badly.

And, at first, this sounds reasonable. Surely there is a point where enough is enough?

Yet since then, scores of larger, faster, and safer cruise liners have crossed oceans without (much) ado.

Hubris was partially to blame. However, as historians are quick to interject, White Star never said the Titanic was unsinkable (sensationalist claims of invincibility by journalists were honed in on after the disaster). The blame should go on the failure to heed warnings. These mistakes are being repeated with the crisis of the twenty-first century.

Long-time subscribers are familiar with the Silver Tsunami. As undeniably destructive as it will be if longevity research is not vigorously pursued, countless Edward Smiths continue to turn a blind eye, even when they themselves are feeling the toll aging eventually takes on us all.

You already know we need to act now. Nothing can be done once we've veered too far off course, besides sit back and watch the greatest societal implosion in history.

Today an aptly named bacterium, Halomonas titanicae, is devouring the shipwreck. The scene could be interpreted through the lens of memento mori, a moldering display of what is destined to become of us all, or it could be seen for what it is: a showcase of nature's ingenuity, which is hardly separate from our own.

“Nature, to be commanded, must be obeyed.”

 - Francis Bacon

Gene therapy gives us the power to influence life at its most basic level. Nothing is more natural. Gene therapy does not defy nature like a petulant child but works with it (and through it) to achieve very human (and humane) ends. It is, as we've explored in our latest Medium article, our most majestic and tireless teacher.

Please support our mission of ending dementia and other age-related diseases today. 

References and Suggested Reading

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Begley, Sharon, et al. “The Maddening Saga of How an Alzheimer's 'Cabal' Thwarted Progress toward a Cure for Decades.” STAT, 30 Dec. 2019, https://www.statnews.com/2019/06/25/alzheimers-cabal-thwarted-progress-toward-cure/.

Booth, Heather DE, Warren D. Hirst, and Richard Wade-Martins. “The role of astrocyte dysfunction in Parkinson's disease pathogenesis.” Trends in neurosciences 40.6 (2017): 358-370.

Blackburn, Daniel, et al. “Astrocyte function and role in motor neuron disease: a future therapeutic target?.” Glia 57.12 (2009): 1251-1264.

Cagnin, Annachiara, et al. “In-vivo measurement of activated microglia in dementia.” The Lancet 358.9280 (2001): 461-467.

Collado, Manuel, Maria A. Blasco, and Manuel Serrano. “Cellular senescence in cancer and aging.” Cell 130.2 (2007): 223-233.

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Hansen, David V., Jesse E. Hanson, and Morgan Sheng. “Microglia in Alzheimer's disease.” Journal of Cell Biology 217.2 (2017): 459-472.

Hemonnot, Anne-Laure, et al. “Microglia in Alzheimer disease: Well-known targets and new opportunities.” Frontiers in aging neuroscience 11 (2019): 233.

Hochstrasser, Tanja, Josef Marksteiner, and Christian Humpel. “Telomere length is age-dependent and reduced in monocytes of Alzheimer patients.” Experimental gerontology 47.2 (2012): 160-163.

“Telomere Length Shortening and Alzheimer Disease - A Mendelian Randomization Study” JAMA Neurol. 2015;72(10):1202-1203, online first 12 October 2015, DOI: 10.1001/jamaneurol.2015.1513.

Panossian, L. A., et al. “Telomere shortening in T cells correlates with Alzheimer's disease status.” Neurobiology of aging 24.1 (2003): 77-84.

Sewell, P. E., et al. "Safety Study of AAV hTert and Klotho Gene Transfer Therapy for Dementia." J Regen Biol Med 3.6 (2021): 1-15.

staff, Science X. “Causal Link between Telomere Shortening and Alzheimer's Disease.” Medical Xpress - Medical Research Advances and Health News, Medical Xpress, 13 Oct. 2015, medicalxpress.com/news/2015-10-causal-link-telomere-shortening-alzheimer.html.

Siracusa, Rosalba, Roberta Fusco, and Salvatore Cuzzocrea. “Astrocytes: role and functions in brain pathologies.” Frontiers in pharmacology 10 (2019): 1114.

Tobin, Matthew K., et al. “Human Hippocampal Neurogenesis Persists in Aged Adults and Alzheimer's Disease Patients.” Cell stem cell 24.6 (2019): 974-982.

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Wolf, Susanne A., Andre Melnik, and Gerd Kempermann. “Physical exercise increases adult neurogenesis and telomerase activity, and improves behavioral deficits in a mouse model of schizophrenia.” Brain, behavior, and immunity 25.5 (2011): 971-980.

Zhao, Ruohe, et al. “Microglia limit the expansion of β-amyloid plaques in a mouse model of Alzheimer's disease.” Molecular neurodegeneration 12.1 (2017): 47.

Zhang, Jianmin, et al. “Telomere dysfunction of lymphocytes in patients with Alzheimer disease.” Cognitive and Behavioral Neurology 16.3 (2003): 170-176.