November 28, 2010
Gene Prevents Alzheimer's Disease In Mice

The mouse conspiracy to cure themselves of all diseases continues apace.

SAN FRANCISCO, CA—November 21, 2010— Scientists at the Gladstone Institute of Neurological Disease (GIND) in San Francisco have discovered a new strategy to prevent memory deficits in a mouse model of Alzheimer's disease (AD). Humans with AD and mice genetically engineered to simulate the disease have abnormally low levels of an enzyme called EphB2 in memory centers of the brain. Improving EphB2 levels in such mice by gene therapy completely fixed their memory problems. The findings will be published in the November 28 issue of the journal Nature.

Just for the sake of argument imagine that a gene therapy delivered to every brain cell could raise levels of EphB2 and thereby prevent Alzheimer's Disease. Okay, will this even be practical to do anything in the next few decades?

Sound easy? Hold on. The human brain has about 100 billion neurons (to be fair some estimates are down in the range of 10's of billions of neurons). Well, okay, how to deliver exactly 1 copy of a gene to 100 billion cells all sitting behind barriers designed to protect them? Even if we could get thru the barriers how to prevent some cells from getting dozens or hundreds of copies of a gene before other cells get any? That's not just a rhetorical question (though rhetorical questions are great and I encourage their use). I'd like to know how to approach the problem.

One can break this up: How to package the genes so they can get into cells? How to structure the inner portion of the package so the delivered genes will either integrate into the host genome without causing damage or otherwise situate themselves to function well for an extended period of time? How to get the genes into neurons that are, for whatever reason, harder to reach? Finally, how to prevent overdosing? Is overdosing the hardest and most serious problem? Maybe a delivered package could include code for machinery that would break down a newly arriving second package. But that would take a lot of work to make such a specific extra bit of functionality and might make the delivered package too big.

As I always bring up when I read debates about when we will be able to rejuvenate our bodies and greatly extend human lifespans, brain rejuvenation is the hardest part. We can't replace our nerves without replacing who we are. We need to fix them in place. Gene therapy, nano repair bots, and helper cell therapies (e.g. new glial cells) will all be needed for this purpose. I do not think that gene therapy and helper cell therapy by themselves will be sufficient in the long run. But if we are lucky then we can extend our brains for, say, an extra 50 years to give time for the nanobots to be developed. If we are not so lucky then we'll become a society of young bodies and senile minds.

Share |      Randall Parker, 2010 November 28 12:36 PM  Brain Alzheimers Disease

Xenophon Hendrix said at November 28, 2010 12:45 PM:

Is it theoretically possible to replace neurons a few at a time so that new neurons get integrated into old memories and learning?

Randall Parker said at November 28, 2010 5:47 PM:


Possibly there's redundancy in the memory storage. Possibly the brain has the ability to copy memories to additional places. But suppose this is true. How to only knock out one of, say, 3 copies of some memory? We'd need to know where each copy of each memory is. Seems harder than developing the means to repair neurons.

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