Researchers at Yale University found that stress in rats blocks the activity of a gene that promotes healthy neural connections in the brain. The findings, published yesterday in Proceedings of the National Academy of Sciences, suggest that activating the gene (neuritin, which functions similarly in humans) led to an effect that protected against both depression and the brain atrophy associated with depression. Said an author, “there’s good evidence there’s a loss of synaptic connections in depressed rodents and depressed patients. If you don’t have the appropriate number of connections in synapses, your brain isn’t going to function properly.”
Son, H., Banasr, M., et al; “Neuritin produces antidepressant actions and blocks the neuronal and behavioral deficits caused by chronic stress,” Proceedings of the National Academy of Sciences, online June 25, 2012
Stress-Induced Depression Is Real
Stress Blocks Gene That Guards Brain Against Depression
Connection found between gene and depression
Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.
Mad in America has made some changes to the commenting process. You no longer need to login or create an account on our site to comment. The only information needed is your name, email and comment text. Comments made with an account prior to this change will remain visible on the site.
“lack of neuritin causes depression”
No doubt, this ‘scientifically proven truth’ shall soon be acknowledged, the latest chapter in the “chemical imbalance” theory of ‘depression’ – just keep an eye on this entry, in Wikipedia:
Today, there’s no mention of “neuritin”; but, it won’t be long before the Wiki elves add it in there.
These Korean researchers are making a name for themselves.
Kermit, thanks for the links.
Love this optimistic analysis From KoreaTimes.co.kr (06-26-2012 20:31):
“‘The information will be utilized when developing a new anti-depressant with a better efficacy.’”
See more from that article, as I’ve quoted it, somewhat at length…
“The Ministry of Education, Science and Technology said Tuesday that the team led by Hanyang University biomedical science professor Son Hyeon found that a gene called neuritin plays an important role in regulating depression, affected by the activity of hippocampus neurons in the brain.
“The discovery was the result of four years of study on the behavior of white mice which developed depression…”
(Actually, they were Male Sprague–Dawley rats; and, I assure you, they had good reason to be depressed; see the last lines, from this news item, I’ve quoted, below.)
“The findings were published in the June edition of ‘Proceedings of the National Academy of Sciences (PNAS),’ a renowned international science journal.
“‘It is significant that we have found a connection between depression and neuritin, which becomes more active stimulated by neurons,’ said Son.
“‘The information will be utilized when developing a new anti-depressant with a better efficacy.
“According to the Health Insurance Review and Assessment Service, 510,000 Koreans currently have a depressive disorder. The figure is 20 percent up from 2007.
“Korea also has shown the highest suicide rate among member states of the Organization for Economic Cooperation and Development (OECD). Suicide is closely linked to depression.
“The breakthrough in research that has found the link between the gene and depression is likely to have a positive effect on the treatment of the increasing number of people suffering from depression.
“Depression is a mental disorder that is widespread among the public, regardless of age and gender. The disorder had been found to occur when the function and structure of the neuron in the hippocampus contracts.
“However, there had been no evidence on how the phenomenon was actually related to depression and what kind of effect the depression medicine had.
“Based on the fact that neuritin boosts the growth of neuritis, the team had set the hypothesis that the lack of neuritin causes depression and when a large amount is produced, the disorder is alleviated.
“The team had let the white mice develop chronic stress depression by providing two types of aversive stimuli daily for 35 days. The stimuli included trapping the mice in cold water and not giving food…”
From Wikipedia’s entry for Aldous Huxley’s classic dystopian novel, “Brave New World” (1931): “…The State-produced drug, as a self-medicating comfort mechanism in the face of stress or discomfort, thereby eliminates the need for religion or other personal allegiances outside or beyond the World State.”
(That drug was called, “Soma.” Unfortunately, for the Korean research team, that name’s been taken. From Wikipedia’s “Soma” entry: “‘Soma’ is a brand name for the muscle relaxant drug carisoprodol, manufactured and marketed in the United States by Meda Pharmaceuticals. It is used to relieve discomfort associated with painful musculoskeletal conditions such as backache.”)
The researchers’ original sin is supposing the mice develop what even in articulate humans is difficult to define as “depression.”
These giant fanciful leaps in reading mice minds are the foundation of biopsychiatry research.
This is why, when the resulting drugs are applied to humans, they only kinda sorta work, if you squint and look at the data the right way.
Kermit, you can drop this comment which I left at June 26, 2012 at 5:01 pm.
You’ll see I posted successfully at June 26, 2012 at 5:07 pm 🙂
Brain atrophy in depression??? Excuse me?? When did this become a fact?
Note the abstract starts with a questionable premise: “Decreased neuronal dendrite branching and plasticity of the hippocampus, a limbic structure implicated in mood disorders, is THOUGHT to contribute to the symptoms of depression.”
As usual, starting with a false premise leads to conclusions that might hold in an alternate reality.
Biopsychiatry sees humans as psychically equivalent to mice.
I would feel insulted, but they probably underestimate the mice, too.