Stardate 43917.4: the USS Enterprise NCC 1701-D is about to host high-level negotiations with a mysterious and persnickety race known as the Legarans. Representing the Federation: none other than (“how do you vote?”) Sarek of Vulcan, as he was called by the late Tellarite Ambassador Gav. (Sarek is, of course, better known to most as Spock's dad.)
Even by Vulcan standards, Sarek is getting on in years at this point. As soon as he arrives onboard, something strange happens: the crew of the Enterprise start developing extremely short tempers, and it seems nobody's immune.
The unwitting culprit turns out to be none other than Sarek himself, who's been secretly suffering the effects of a rare degenerative condition. Known as Bendii syndrome, it causes Vulcans to gradually lose the emotional control they prize so highly, and since they're mildly telepathic, their repressed feelings can leak out and affect the people around them. Sarek's had a long time to build up a fair amount of inner regret and turmoil, and now it's threatening to sink the entire mission: the Legarans will only meet with him, accepting no substitutes. Fortunately, there's a solution: Sarek mind-melds with Captain Picard, who lends him some of his own considerable self-discipline at the cost of absorbing a little of Sarek's pain and rage. It works. Sarek completes the Legaran negotiations with cool aplomb, while Picard howls in anguish in a dark room with only Dr. Crusher to keep him company. Later, Sarek's ride home arrives, and in the transporter room he and the captain reflect on the bond they now share before parting ways.
No race is immune to the perils of aging, not even fictional ones. But the third-season Star Trek: The Next Generation episode "Sarek" may hit closer to home than most for some of its audience: Bendii syndrome bears a distinct resemblance to a real-world illness that happens to be the sixth-leading cause of death in the United States, none other than Alzheimer's disease. Alzheimer's manifests as a kind of progressive dementia that usually starts with memory loss, then moves on to affect thinking and behavior. Sufferers of Alzheimer's eventually lose the ability to carry on conversations or interact meaningfully with their surroundings.
Unfortunately, no one really knows what causes Alzheimer's disease, which makes treating it an extremely difficult proposition. We know that the symptoms of Alzheimer's are created by the breakdown of neural tissue, but what triggers the breakdown? More importantly, how do we stop it? Unfortunately, it remains a mystery. One theory, called the apoE4 model, says that there's a specific genetic risk factor that causes inhibitory neurons to die off. Inhibitory neurons are one side of an important neuronal coin, the other being excitatory — think of them as your brain's brakes and gas pedals, respectively. In nearly 3/4 of Alzheimer's cases, the problems are caused by a degeneration of inhibitory neurons, throwing off the brain's balance of stimuli. Cut the brake wires on the brain, and everything just goes downhill from there.
On TNG, Bendii Syndrome is similar to Alzheimer’s in the breakdown of neural pathways. Since it's a Vulcan disease, short-term treatments like the Sarek/Picard mind-meld can be effective at restoring emotional control through purely telepathic means, reestablishing order through sheer force of will. But it's not a permanent fix — more like putting a fresh coat of paint on wood that's rotting underneath. The damage continues to progress, and will eventually reassert itself.
But Sarek — indeed, the whole Federation — has apparently never heard of stem cell science. A study from the Gladstone Institutes has revealed that it might be possible to actually re-grow inhibitory neurons, with a little help from regenerative medicine. Researchers from Gladstone and UC San Francisco took mice that exhibited Alzheimer's-like symptoms matching the apoE4 model and transplanted inhibitory neuron stem cells into their brains, just like planting seeds. Incredibly, not only did those seeds survive the transplant process, but they began to grow, essentially replenishing lost inhibitory neurons and restoring missing functions.
The implications are wildly exciting: successful transplants of the same kind in humans could be a meaningful treatment for a significant chunk of Alzheimer's patients — even, dare we say, a framework for an eventual cure. As it happens, we here at XPRIZE are developing a prize competition to incentivize a way to accurately screen, diagnose and treat Alzheimer's disease, with the goal of making it easier to identify and one day cure it in humans worldwide. But if it helps, we won't rule out mind-melds either.
Jon Sung is a contributing writer for XPRIZE and copywriting gun-for-hire to startups and ventures all over the San Francisco Bay area. When not wrangling words for business or pleasure, he serves as the captain of the USS Loma Prieta, the hardest-partying Star Trek fan club in San Francisco.
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