Calico Undertaking Neural Plasticity Drug Research
Probably indicative of the Calico Labs strategy for the foreseeable future, here is a piece of news from last month that I missed at the time. The initiative will be taking over funding of an established drug development program aimed at increasing neural plasticity, trying to find ways to spur the brain to generate more new neurons to compensate for damage. Like much of what goes on in modern medical research for age-related conditions, this is a compensatory approach, addressing proximate rather than root causes of degeneration. For many conditions, this may be useful and possibly even sufficient - Parkinson's disease, for example, affects a mechanical part of the brain that has little to do with the structure of the mind, and the cells there could in theory be replaced wholesale over and again as needed.
Generally, however, we want a research community that works to repair and prevent the root causes of aging, rather than one focused on trying to patch up late stage age-related damage after the fact, or worse, trying to alter the operation of metabolism to make it run slightly better when damaged. If the Calico Labs leadership intend to build an establishment rapidly over the next few years by adopting promising research programs, then the less optimal paths are largely what they'll be funding, however:
This week, UT Southwestern researchers published a new paper about the molecular target of P7C3 compounds, a class that has been shown to help in various animal models of neurodegeneration. UT Southwestern previously licensed the P7C3 compounds to Dallas-based 2M Companies. 2M and Calico have now entered into a new license agreement under which Calico will take responsibility for developing and commercializing the compounds resulting from the research program. Under the agreement, Calico will fund research laboratories in the Dallas area and elsewhere to support the program.Death of nerve cells is the key mechanism in many devastating neurological diseases for which there are currently inadequate treatment options. [The UT Southwestern researchers] have collaborated since 2007 to find novel drugs that promote the growth of new nerve cells in the brain, a process known as "neurogenesis." The P7C3 compounds discovered by the team have previously been shown to be effective in animal models of age-related neurocognitive impairment, Parkinson's disease, amyotrophic lateral sclerosis (ALS), and depression. New research [shows] that these drugs activate a cellular enzyme involved in energy metabolism, known as NAMPT (short for nicotinamide phosphoribosyltransferase), which is critical to the proper functioning and survival of cells. A separate [study] shows that the P7C3 compounds protect against brain dysfunction when given to rodents following traumatic injury.
I would not be surprised that Calico is focusing on restoration or enhancement of neuro-plasticity. Neuro-plasticity is the basis of learning and the Google people, being in the cognitive intensive industry that they are, are obsessed with anything that increases learning ability.
They research on the usual stuff, i've actually talked to one of the researchers, It's just things on understanding why aging happens and how the metabolism works, ect.
Google does not fund SENS because well, they find it bold claims that aren't 100% confirmed. Being enthusiastically outspoken with the risk of whiplash.
To sum it up, yes Calico is getting a lot of money, and some of it will benefit what SENS is doing as some of the things may kind of overlap. But SENS is still the only company that seeks to repair and undo damage, rather then put a band-aid on it. If you intend to not want to die any time soon, then SENS still isn't off the hook yet.
Neural restoration is critical research. Keeping existing neurons alive indefinitely is not plausible, not even in healthy brains. If neurons come back at the same rate that they are lost, the brain is functionally immortal. For treating specific degenerative diseases, the critical part is making the new neurons not susceptible to the same things that quickly killed the old.
It also has the side effect of making any researchers who take it smarter, creating a semi-singularitarian effect.
Like all of us I wish Calico would invest in a more SENS/regenerative approaches which would have a far larger effect on health. That said this research sounds a bit better than the average slow road metabolic tweaking that they mostly research because at least there might be some "new" neurons. (Though they'd probably be less vital than young new cells)
Interestingly, I had a relative with Parkinson's disease and it manifested itself in him as severe dementia but without any real motor problems. From what I've read dementia occurs in a sizable minority of Parkinson's patients. I wonder what effects the P7C3 class of drugs might have on Parkinson's-related dementia, if any.
There is a related article on Buck Institute's blog:
"Breaking NAD: How one metabolite became the biggest story in anti-aging therapy in less than a year." - article that explain why Calico moves that direction.
http://sage.buckinstitute.org/breaking-nad/