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New Antidepressant Discoveries That Might Change

Depression Forever

SOURCE: Pexels

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By JR THORPE Jan 26 2017

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Antidepressants are ripe for a change. Their history has been one of significant
advancement; since the first discovery of tricyclic antidepressants in the 1950s (by accident,
during a tuberculosis trial), we've developed more refined versions, from MAOIs to today's
very popular selective serotonin reuptake-inhibitors (SSRIs). A new age of antidepressant
therapies may well be coming, though, not just in new ingredients, but in how we approach
mood imbalances in the brain.

Antidepressant science is currently booming. Back in July 2016, we saw the beginnings of
genetic and blood testing to get accurate dosage, and we rocked into 2017 with new
information about the possibility of psilocybin, the active ingredient in magic mushrooms, as
a source for future anti-depressant development. (Note that tests on this used psilocybin
itself, not mushrooms, so don't take doses of something from your dealer and hope it'll work;
that's not medically tested.)

Considering the spread of depression worldwide the World Health Organization estimates
that up to 350 million people around the world have it this is hardly a minor-scale issue.
And as science deepens its interest, we're increasingly coming across exciting new
possibilities for the future of depression's treatment, some of which one day might make it
onto our shelves and into our homes.

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The New Development Causing A Fuss

SOURCE: GIPHY

This week, Finnish scientists announced an exciting breakthrough in their studies of

depression that might provide a new approach to anti-depressants in the future. They
centered their attention on neurogenesis, the production of new nerve cells in the brain,

which previous research has shown might play a role in anxiety and depression in the brain's
hippocampus: it seems to be impaired in those with certain mood disorders.

They found that a particular kind of protein, Jun N-terminal kinases (or JNK), is responsible
for moderating neurogenesis in the hippocampus, and so seems directly responsible for
anxious and depressive behavior. When they fiddled with it, they found that inhibiting it
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anxious and depressive behavior. When they fiddled with it, they found that inhibiting it
produced positive mood responses: the mice with their JNK inhibited had lower anxiety
levels and more neurogenesis. And by "more" they mean "much more:" cell proliferation,
they reported, "increased by 80% and survival by 200% at 6 weeks" after the JNK treatment.
The scientists think that the combination of JNK inhibition and the new bunch of cell growth
produces a "powerful neurogenic stimulus" that helps mood disorders.

This is particularly intriguing because JNK is at the forefront of a variety of disease studies. In
a 2003 study called, hilariously, "From Junk To Gold," JNK inhibition was mentioned to be
possibly helpful for "inflammatory, vascular, neurodegenerative, metabolic and oncological
diseases in humans," and now we might be able to add mood disorders to that list. It's a
complete departure from the tendency of antidepressants to target neurotransmitters, but
what a protein inhibitor pill would look like, and how it would work in humans, remains
unknown. Stay tuned.

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We May Soon Be Able To Tell In Advance Which Drugs Will

Work Best

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SOURCE: GIPHY

Wouldn't it be useful if we knew whether a particular kind of antidepressant would work

before somebody started a course on it? We might be able to. A particular kind of brain
processing pattern detectable in MRIs is, according to new science from the University of
Illinois, a sign that normal anti-depressant therapy won't be effective in a patient. The
pattern, interestingly enough, pops up when we make an error, and shows communication
between parts of the brain associated with mistake detection and information processing.
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between parts of the brain associated with mistake detection and information processing.

Thirty-six adult patients with depression and no drug regime were given a series of tests
while having an MRI, then given varieties of antidepressants and monitored over months for
the usefulness of the treatment. Interestingly, there was a high correlation between those
patients who showed the brain pattern in response to error and those who showed little
response to traditional drug treatment.

The pattern itself, the scientists suggest, may be demonstrating a powerful tendency to
"ruminate" over mistakes or make negative inferences from them. The depression-
rumination cycle, the American Psychological Association says, is a key component of
serious depressive disorder, in which negative experiences and self-talk are constantly
reiterated and revisited in the brain, depleting mood. Traditional antidepressants don't really
target rumination behavior, but an overview of the next wave of antidepressants in 2013
noted that ketamine shows promise as a possible treatment for it in depressives. If enough
of these therapies develop in tandem, brain scans can help depressives be placed onto
drugs that accurately reflect the specific patterns of their mood disorders, and so have better
experiences.

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Arthritis Drugs May Help Antidepressant Response

SOURCE: GIPHY

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The world of options opening up to those who aren't responding to antidepressants doesn't
require entirely new drugs, though. At least that's according to a bit of science released in
November 2016, in which bipolar people in the depressive phase of their disorder who had
previously been unresponsive to antidepressants were helped by an unexpected source: an
arthritis drug.

Celecoxib, an anti-inflammatory drug given to arthritis sufferers, was given to a portion of the
study group alongside the antidepressant Lexapro, while the other portion was given
Lexapro and a placebo. After a few weeks, 45 percent of the placebo group reported a
significant lift in their depression and 10 percent indicated it had gone away completely. But
that was dwarfed by the experiences of the celecoxib group: 78 percent of them
experienced a massive drop in their depressive symptoms, while 63 percent reported its
total removal. That's massive.

The scientists behind the test think it has to do with the role of inflammation in
neurotransmitter performance. Neurotransmitters are the things targeted by SSRIs like
Lexapro, and significant science has already been done linking chronic low-grade
inflammation in the body to experiences of depression. The anti-inflammatory effects of
celecoxib banished the inflammation, helped neurotransmitter improve their performance,
and kicked depression out of the ballpark.

This is cool because it's a therapy that can actually be useful now. Tests for low-grade
inflammation do exist, so if your antidepressant isn't working sufficiently and you have a
doctor willing to look at the latest science, they might be able to test you for it and
experiment with adding arthritis drugs to your dosage. It's a highly experimental therapy that
needs to be undertaken carefully (and note that the study only involved bipolar people, not
people with major depressive disorder), but it's a very interesting start.

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