Word: braining
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When it comes to Alzheimer's disease, there hasn't been much to celebrate in recent years. Efforts to develop a vaccine against the brain disorder have stalled, and no drugs have been able to reverse the slow death of neurons that robs people of their memories and thoughts. For the first time in many years, however, researchers in the field are genuinely excited about the potential for effective drug treatments and helpful new risk factors...
...some of the conference's most exciting papers. Researchers from Mount Sinai School of Medicine reported, for example, that compared with other Alzheimer's patients, those who had diabetes and took insulin plus another anti-diabetes medication to control blood sugar had 80% fewer amyloid plaques - the sticky brain-clogging masses that, together with protein tangles, are the hallmarks of Alzheimer's disease. Although the mechanism wasn't entirely clear, researchers think the drugs may work by normalizing the brain's communication network of insulin receptors, which goes awry in the Alzheimer's brain, while clearing away the damaging plaques...
Exactly how that drive plays out in the body is still a mystery. There are two theories, Lightfoot says: Genes may affect either the way muscles work - perhaps causing them to use energy more efficiently and preventing fatigue - or some higher-order biochemical circuit in the brain, such as levels of the neurotransmitters dopamine or serotonin. Researchers have examined the muscle tissue of the mice in the study, however, and early data, which has not yet been published, suggests that there's no difference in their function. So the researchers' best guess is that the drive to exercise...
Compared with patients who never developed diabetes, patients who had the disease but took insulin along with one additional medication to control blood sugar (typically metformin or glyburide) had 80% fewer brain-clogging amyloid plaques in their brain. Build up of these protein plaques, which are one of the hallmarks of Alzheimer's disease, can interfere with normal communication between nerve cells and cause deficits in memory and cognition. "The group on combination therapy had a very, very low load of neuritic plaques," Beeri says. "Their brains looked almost like normal people." The medications did not, however, do much...
Beeri and her group are already trying to figure out how - and why - the combination therapies might curb plaque formation but leave the tangles alone. One theory is that the drugs normalize the communication network of insulin receptors, which go awry in the Alzheimer's brain, somehow restoring those pathways to as close to normal as possible, while clearing out the damaging plaques that form when the network malfunctions. "Our hypothesis is that with the combination therapy, the gene and protein expression of these Alzheimer's patients might be close to that of normal people who don't have Alzheimer...