Learning a second language is easiest at seven. Muscular strength peaks in our mid-twenties (and remains at this high for approximately a decade).

But there's no need to be sad.

Other skills, like arithmetic, are mightiest at fifty and our vocabularies don't reach their zenith until our seventies. Similarly, our emotional intelligence takes time to mature, becoming most formidable at fifty.

These fun facts aside, aging is undeniably bad for our brains. Whether it results in “normal” cognitive decline, or something more insidious, the same molecular processes that affect our other organs can wreak havoc on our minds.

Youth and experience are not opposites. As regenerative medicine makes greater headways, this will become clearer by the day.

Maybe in the future we will have experienced minds within young brains…

To see this future, we are building on the success of the first human dementia study.

Please support this initiative by sharing this link with friends, family, and relevant organizations. The first study provided compelling evidence for safety and efficacy (Sewell, 2021). Our second is poised to be the largest of its kind, another milestone for longevity research made possible by BioViva.

Scientists can fall prey to the same mistakes as anyone. For thirty years, as STAT puts it, a “cabal” has controlled the direction of dementia research (Begley, 2021). Note that word is singular; there were not teams scouring every angle for insights. No, the cabal chose a single road and followed it into a blind alley. The author states:

"In the 30 years that biomedical researchers have worked determinedly to find a cure for Alzheimer's disease, their counterparts have developed drugs that helped cut deaths from cardiovascular disease by more than half, and cancer drugs able to eliminate tumors that had been incurable. But for Alzheimer's, not only is there no cure, there is not even a disease-slowing treatment.”

They are not evil people and (not necessarily) bad researchers, but they are working with an outmoded paradigm. Attempting to treat age-related diseases without addressing the aging process is pointless. It's like building a plane while pretending gravity doesn't exist.

How many school children have Alzheimer's?

College kids?

People in their forties? Some, but it is rare and the result of a single genetic defect.

Biological aging is the single greatest risk factor for all forms of dementia.

In our latest Medium article, a brief but thorough overview of the comparative biology of aging (animal lovers rejoice), we explore why aging is, in all likelihood, a programmed phenomenon.

Drawing inspiration from the natural world, we also look into the different mechanisms animals have evolved to improve their longevity.

If this is the case, why does anyone need to age?

Evolutionary and comparative biology may seem far removed from our daily lives, but how we think about them influences policy makers, governments, universities, companies, and individuals.

Proposals to do anything about aging were quickly dismissed for decades. In many circles, despite the sizable evidence to the contrary (and the unaffordability of doing nothing), it is still considered a vain pursuit.

This is why initiatives like our second dementia study are so crucial. By showing the efficacy of our approach, we can change public opinion. It is also why your efforts are critical. Everything written and said about longevity research has the potential to move it forward or backwards.

Aging and disease are problems that eventually affect us all. We are all in this together. 

References and Suggested Reading

Akiyama, Haruhiko, et al. “Inflammation and Alzheimer's disease.” Neurobiology of aging 21.3 (2000): 383-421.

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.

Mu, Yangling, and Fred H. Gage. “Adult hippocampal neurogenesis and its role in Alzheimer's disease.” Molecular neurodegeneration 6.1 (2011): 85.

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.

Versijpt, Jan J., et al. “Assessment of neuroinflammation and microglial activation in Alzheimer's disease with radiolabelled PK11195 and single photon emission computed tomography.” European neurology 50.1 (2003): 39-47.

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.