Wednesday, 8 March 2017

Immortality for All


Recent advances in gene therapy accelerated by CRISPR (clustered regularly interspaced short palindromic repeats) low cost gene editing technology have shed light upon a new means of extending life; potentially indefinitely!

It has been known for some time that continuous blood transfusion from young to elderly clones rejuvenates life:
Parabiosis is a 150-year-old surgical technique that unites the vasculature of two living animals. (The word comes from the Greek para, meaning 'alongside', and bios, meaning 'life'.) It mimics natural instances of shared blood supply, such as in conjoined twins or animals that share a placenta in the womb.

...With neuroscientist Robin Franklin at the University of Cambridge, UK, her team showed that young blood promotes repair of damaged spinal cords in older mice. With Harvard neuroscientist Lee Rubin, she found that young blood sparks the formation of new neurons in the brain and olfactory system. And with cardiologist Richard Lee at Brigham and Women's Hospital in Boston, Massachusetts, she found that it reverses age-related thickening of the walls of the heart.

...In the heart, brain, muscles and almost every other tissue examined, the blood of young mice seems to bring new life to ageing organs, making old mice stronger, smarter and healthier. It even makes their fur shinier.
-- "Ageing research: Blood to blood" - Nature
In March of this year, using CRISPR editing of bone marrow and gene therapy, a French teenager after 15 months without recurrent symptoms was declared cured of sickle cell disease:
The world-first procedure at Necker Children's Hospital in Paris offers hope to millions of people with the blood disorder.

Scientists altered the genetic instructions in his bone marrow so it made healthy red blood cells.

So far, the therapy has worked for 15 months and the child is no longer on any medication.
-- "Teenager's sickle cell reversed with world-first therapy" - BBC.
Professor Hartmut Geiger's recent work defeating cancer required transplanting bone marrow between mouse clones, applying gene therapy to ensure donated bone marrow stem cells were more proliferate:
"We show that the place where HSCs [hematopoietic stem cells] form in the bone marrow loses osteopontin upon aging, but if you give back the missing protein to the blood-forming cells they suddenly rejuvenate and act younger," says Hartmut Geiger, PhD.
-- "Scientists wage fight against aging bone marrow stem cell niche" - Science Daily.
The professor's work specifically identifies osteopontin in the prevention of HSCs:
Upon aging, hematopoietic stem cells (HSCs) undergo changes in function and structure, including skewing to myeloid lineages, lower reconstitution potential and loss of protein polarity. While stem cell intrinsic mechanisms are known to contribute to HSC aging, little is known on whether age‐related changes in the bone marrow niche regulate HSC aging. Upon aging, the expression of osteopontin (OPN) in the murine bone marrow stroma is reduced. Exposure of young HSCs to an OPN knockout niche results in a decrease in engraftment, an increase in long‐term HSC frequency and loss of stem cell polarity. Exposure of aged HSCs to thrombin‐cleaved OPN attenuates aging of old HSCs, resulting in increased engraftment, decreased HSC frequency, increased stem cell polarity and a restored balance of lymphoid and myeloid cells in peripheral blood. Thus, our data suggest a critical role for reduced stroma‐derived OPN for HSC aging and identify thrombin‐cleaved OPN as a novel niche informed therapeutic approach for ameliorating HSC phenotypes associated with aging.
-- "Osteopontin attenuates aging‐associated phenotypes of hematopoietic stem cells" - EMBOpress
Since blood is created within bone marrow, using gene therapy to make the younger donor bone marrow more proliferate presents a way of restoring osteopontin expression and subsequently youth. A way to cure mortality, eventually inexpensively.




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