By: Pari Heidari, Larry King Now
A brand new study published this week in Science links Alzheimer’s to a defective immune system process. The study, performed on mice and led by neurologist Beth Stevens at Boston Children’s Hospital, shows that a specific set of proteins and cells, aiding the immune system by “pruning” excess synapses in the brain, can become overactive and start deconstructing nerve cell connections unnecessarily. The findings are groundbreaking in that they directly contradict earlier theories that claimed the increased microglia and C1q activity (the cells and proteins designated to aid the immune defense in our central nervous system) were part of a reaction to other mechanisms, and not a potential cause.
Stevens describes the process, stating, “instead of nicely whittling away [at synapses], microglia are eating when they’re not supposed to.”
Edward Ruthazer, neuroscientist at the Montreal Neurological Institute and Hospital in Canada, says the research is still quite controversial, but that “it’s difficult to argue with the strength of the study’s evidence.”
Understanding the role of microglia and C1q in the development of Alzheimer’s could turn out to be crucial. In fact, Stevens says she suspects the overactive synaptic pruning of perfectly healthy brain connections could well be the cause of other brain disorders.
Alzheimer’s is a degenerative disease that is all too familiar to many of us. It is estimated that around 5.3 million Americans suffer from this terrible condition.
Up till now, over 99% of clinical trials for a drug have proven unsuccessful. This study adds to a growing body of research that supports the theory that excessive synaptic pruning is the faulty, culpable mechanism.
Want to know more about Alzheimer’s disease? Check out the video below to hear what the “Father of neuroscience,” Dr. Michael Merzenich, had to say about delaying -- and even reversing -- the onset of Alzheimer’s with targeted brain exercises.
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