14 DAY TRIAL // Sirtuins are members of a class of proteins that play an important role in promoting longevity. They also help regulate stress responses in species ranging from mice and yeast to humans, and researchers believed they had a fairly good grasp on all effects these molecules elicited in the human body. However, a recently-published investigation determined that sirtuins also play a fundamental role in suppressing the most important molecules underlying Alzheimer's, called amyloid beta proteins, PhysOrg reports.
These molecules clump together to form with is known as plaques in the brain. These structures prevent the electrical signals with which nerve cells communicate from reaching the end of the neural pathway they were fired on. This is why Alzheimer's is cataloged as a neurodegenerative condition. With time, the effects these plaques produce become increasingly severe, until the brains of patients can no longer cope with the damage.
The investigation that came to the new conclusion was conducted by investigators at the Massachusetts Institute of Technology (MIT), who determined the additional roles sirtuins play in the body. According to MIT professor Leonard Guarente, who led the research group, it would appear that the discovery may in the near future be used to underlie the development of a host of new therapies aimed at treating Alzheimer's. Over the past decade, progress in understanding and treating the condition has been relentless. But a lot of work still remains to be done, experts agree.
The MIT group conducted its work on a batch of genetically-altered mice that had been engineers so as to express Alzheimer's symptoms. The scientists learned that, by injecting the unsuspecting creatures with the sirtuin-class protein SIRT1, the evolution of the neurodegenerative condition could be prevented. It remain to be seen whether the effect holds in humans as well. A lot of testing still lies ahead before human trials can begin. Details of the work appear in the July 23 issue of the esteemed scientific publication Cell.