Schizophrenia Study May Have Revealed Its Cause

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Schizophrenia Study May Have Revealed Its Cause

With over two million Americans alone suffering from the disease, this landmark study could have far reaching implications for many. (“No it won’t, says the voice in my head)

No real treatment, just a muting of schizophrenia symptoms

As someone who suffers from clinical depression, is a bit mad by my own diagnosis and has been diagnosed as bi-polar disease in the early 80s, I struggle to imagine a life characterized by hallucinations, and delusional thinking. (Never mind believable voices in my head)

I wasn’t making light of the disease by any means earlier and was heartened by today’s findings that were reported today following a landmark study. Those findings were published in the journal Nature. Despite, seemingly daily, medical advances schizophrenia as largely baffled the medical community since it was first given a name. While it won’t lead to immediate aid to sufferers of the disorder, it could be a touchstone for researchers looking for a solution going forward into the future.

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“They did a phenomenal job,” said David B. Goldstein, a professor of genetics at Columbia University speaking to the New York Times. Goldstein has not been a fan of studies that, in the past, looked into the genetics of mental illness. “This paper gives us a foothold, something we can work on, and that’s what we’ve been looking for now, for a long, long time.”

The study spoke to a process called synaptic pruning that effectively has the brain deciding (on its own) which redundant or weak neural relationships its no longer interest in having in its life. The study essentially concluded that sufferers of the disorder have genes that speed up this pruning.

Who was involved?

The Harvard Medical School, the Broad Institute and the Boston Children’s Hospital all contributed Boston-based researchers and scientists to this endeavor to determine the roots of a disorder that affects so many. The researchers immediately put their focus on the MHC, a spot on the human genome that has been most associated with the disorder in past genetic studies.

“The MHC is the Freedom Tower” of the Manhattan plot, said Eric S. Lander, the director of the Broad Institute. “The question was, what’s in there?”

The answer might be too many variants in a gene called C4 which the group focused on through advanced statistical analysis. Those variations include two proteins, C4-A and C4-B.

“C4-A seemed to be the gene driving risk for schizophrenia,” said co-lead researcher Steven McCarroll, an associate professor of genetics at Harvard , “but we had to be sure.”

Their research led to the conclusion that too much C4-A accelerates synaptic pruning that begins in earnest around puberty. Essentially, too much C4-A is like having an inexperienced teenager clip your hedges, but the hedges is your brains interaction with necessary neurons.

“The finding connects all these dots, all these disconnected observations about schizophrenia, and makes them make sense,” Dr. McCarroll said explaining the dots as the reason that the disorder generally sets in in the adolescent years.

Updated on

While studying economics, Brendan found himself comfortably falling down the rabbit hole of restaurant work, ultimately opening a consulting business and working as a private wine buyer. On a whim, he moved to China, and in his first week following a triumphant pub quiz victory, he found himself bleeding on the floor based on his arrogance. The same man who put him there offered him a job lecturing for the University of Wales in various sister universities throughout the Middle Kingdom. While primarily lecturing in descriptive and comparative statistics, Brendan simultaneously earned an Msc in Banking and International Finance from the University of Wales-Bangor. He's presently doing something he hates, respecting French people. Well, two, his wife and her mother in the lovely town of Antigua, Guatemala. <i>To contact Brendan or give him an exclusive, please contact him at [email protected]</i>
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