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Stress Changes The Brain, And This Could Be How It Happens

The results of a new brain imaging study may have just answered a big question about how stress changes the brain. Using a combination of genetic editing and brain scanning in mice, researchers found that stress triggers a chemical cascade that radically changes how brain networks communicate, and the results could sharpen our understanding of anxiety disorders in humans.

Breaking down the research

Stress serves an important purpose in preparing us to react to danger. Anything the brain perceives as threatening triggers multiple brain networks to synchronize and communicate, all in just a fraction of a second. With systems humming, we make immediate decisions to survive the threat.

But what facilitates all of those brain networks to connect and communicate? That’s been a difficult question to answer in the human brain, because doing so would require examining brain function during the split-second window of facing a threat.

Enter our friends the mice to help solve the problem. Researchers followed a trail of previous studies and zeroed in on the neurotransmitter noradrenaline (aka norepinephrine, a chemical that floods the brain during stress) as a likely facilitator of brain-network connectivity.

The twist was that they had genetically manipulated the rodents’ brains to allow for selectively controlling when noradrenaline was released (not possible in human brains). While controlling the chemical faucet, they also scanned the mouse brains using fMRI to see what would happen.

And what happened, it turns out, was pretty amazing. The release of noradrenaline “rewired” the mouse brains, allowing different brain networks to instantly cross-communicate. But the neurotransmitter wasn’t just facilitating communication, it was restructuring neural connections beyond anyone’s expectations.

“I couldn’t believe that we were seeing such strong effects,” said the study’s first author Valerio Zerbi, a brain imaging specialist from the University of Zurich.

The researchers found the strongest rewired effects in brain areas responsible for processing sensory stimuli (auditory and visual, for example), and in the amygdala, the epicenter of the brain’s threat response system.

What does this mean for us?

It’s the part about threat response that may hold the most promise for better understanding what stress does to our brains.

Allowing for the fact that this was research in mice, the particular dynamic studied here is probably quite similar between us and our rodent counterparts. If noradrenaline rewires the human brain as it appears to rewire the brains of mice, it’s possible the long-term effects of stress are more profound than we’ve realized.

Previous research has linked the flood of noradrenaline to changes in brain connectivity, but it seems likely we’ve underestimated the effects, especially in the small but powerful part of our brain sitting at the center of anxiety disorders: the amygdala.

At a minimum, this research opens new doors for better understanding how both acute and chronic stress effects the brain, and could enlighten new ways of deconstructing anxiety conditions, now the most prevalent mental health disorders worldwide. The study was published in the journal Neuron.

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David DiSalvo is the author of the best-selling book “What Makes Your Brain Happy and Why You Should Do the Opposite”, which has been published in 15 languages, and the books “Brain Changer: How Harnessing Your Brain’s Power to Adapt Can Change Your Life” and “The Brain in Your Kitchen”. His work has appeared in Scientific American Mind, Forbes, Time, Psychology Today, The Wall Street Journal, Slate, Esquire, Mental Floss and other publications, and he’s the writer behind the widely read science and technology blogs “Neuropsyched” at Forbes and “Neuronarrative” at Psychology Today. He can be found on Twitter @neuronarrative and at his website, daviddisalvo.org. Contact him at: disalvowrites [at] gmail.com.

Source: Stress Changes The Brain, And This Could Be How It Happens

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Can NanoTechnology Help Treat Alzheimer’s – Ileana Varela

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Alzheimer’s disease (AD) is the most common form of dementia. It takes a devastating toll on patients and family members, who are usually the caregivers. Current drugs only treat symptoms of AD, not its causes.

FIU researchers are studying a new approach to treating Alzheimer’s using nanotechnology aimed at reducing the inflammation in the brain.

“Current drugs affect neuro-transmitters in the brain. However, inflammation is still clearly present in patients with AD—and seems to be a root cause,” says Madhavan Nair, associate dean for biomedical research and vice president for nanotechnology at Herbert Wertheim College of Medicine.

According to the Alzheimer’s Association, more than 5 million Americans are living with Alzheimer’s; someone in the U.S. develops the disease every 66 seconds; and it is the 6th leading cause of death in the United States – killing more people than breast cancer and prostate cancer combined. June is Alzheimer’s and Brain Awareness Month.

Nair and his team will target brain cells called microglia and will use his FIU patented MENs (magneto electric nanoparticles) carrier system for the specific delivery and sustained release of two
anti-inflammatory drugs, Withaferin A and CRID3, into those cells.

“We are hoping that this will inhibit the neuroinflammatory response in microglia and thus help to improve cognitive function in AD patients,” Nair says. The study is funded by a $224,643 grant from the Florida Department of Health.

Although scientists are not sure what causes cell death and tissue loss in the Alzheimer’s brain, they suspect plaques and tangles are to blame. The plaques form when protein pieces called beta-amyloid clump together between nerve cells (neurons) in the brain.

Investigators in Nair’s lab are using sophisticated technology –bioinformatic tools and 3D structure of beta-amyloid – to find the binding site of these anti-inflammatory drugs on beta-amyloid. These studies could translate into new therapies in the treatment of Alzheimer’s.

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