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neurodegenerative disorders

Brain Imaging: Tackling Chronic Traumatic Encephalopathy

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Brain scans of CTE and AD

Caption: Left to right, brain PET scans of healthy control; former NFL player with suspected chronic traumatic encephalopathy (CTE); and person with Alzheimer’s disease (AD). Areas with highest levels of abnormal tau protein appear red/yellow; medium, green; and lowest, blue.
Credit: Adapted from Barrio et al., PNAS

If you follow the National Football League (NFL), you may have heard some former players describe their struggles with a type of traumatic brain injury called chronic traumatic encephalopathy (CTE). Known to be associated with repeated, hard blows to the head, this neurodegenerative disorder can diminish the ability to think critically, slow motor skills, and lead to volatile, even suicidal, mood swings. What’s doubly frustrating to both patients and physicians is that CTE has only been possible to diagnose conclusively after death (via autopsy) because it’s indistinguishable from many other brain conditions with current imaging methods.

But help might be starting to move out of the backfield toward the goal line of more accurate diagnosis. In findings published in the journal PNAS [1], NIH-supported scientists from the University of California, Los Angeles (UCLA) and the University of Chicago report they’ve made some progress toward imaging CTE in living people. Following up on their preliminary work published in 2013 [2], the researchers used a specially developed radioactive tracer that lights up a neural protein, called tau, known to deposit in certain areas of the brain in individuals with CTE. They used this approach on PET scans of the brains of 14 former NFL players suspected of having CTE, generating maps of tau distribution throughout various regions of the brain.


Alzheimer’s-in-a-Dish: New Tool for Drug Discovery

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Alzheimer's Disease in a dish

Caption: A plaque (orange) disrupts the normal network of human neurons (green) grown in a three-dimensional gel in the lab, mimicking the brain anatomy of Alzheimer’s patients.
Credit: Doo Yeon Kim and Rudolph E. Tanzi, Massachusetts General Hospital/ Harvard Medical School

Researchers want desperately to develop treatments to help the more than 5 million Americans with Alzheimer’s disease and the millions more at risk. But that’s proven to be extremely challenging for a variety of reasons, including the fact that it’s been extraordinarily difficult to mimic the brain’s complexity in standard laboratory models. So, that’s why I was particularly excited by the recent news that an NIH-supported team, led by Rudolph Tanzi at Boston’s Massachusetts General Hospital, has developed a new model called “Alzheimer’s in a dish.”

So, how did Tanzi’s group succeed where others have run up against a brick wall? The answer appears to lie in their decision to add a third dimension to their disease model.  Previous attempts at growing human brain cells in the lab and inducing them to form the plaques and tangles characteristic of Alzheimer’s disease were performed in a two-dimensional Petri dish system. And, in this flat, 2-D environment, plaques and tangles simply didn’t appear.


Protein Pile-up: Common Cause of Brain Disease

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Two images, one dark, one bright, resembling a finger.

Caption: Left: High levels of the toxic ataxin-1 protein have destroyed nerve cells in the cerebellum of a mouse, causing a severe disease. Right: Here researchers have genetically blocked the genes that normally produce high levels of ataxin-1. This prevents the disease from developing and keeps the brain healthy.
Credit: Harry Orr, Department of Laboratory Medicine and Pathology, University of Minnesota

With our aging population, more people are developing neurodegenerative disorders like Alzheimer’s and Parkinson’s disease. We currently don’t know how to prevent or cure these conditions, and their increasing prevalence not only represents a tragedy for affected individuals and their families, but also a looming public health and economic crisis.

Even though neurodegenerative diseases have varied roots—and affect distinct cell types in different brain regions—they do share something in common. In most of these disorders, we see some type of toxic protein accumulating in the brain. It’s as if the brain’s garbage disposal system is blocked, letting the waste pile up. In Huntington’s disease, huntingtin is the disease-causing protein. In spinocerebellar ataxia, it’s the ataxins. In Alzheimer’s, it’s beta-amyloid; in Parkinson’s, it’s α-synuclein. When garbage builds up in your kitchen, it’s a bad situation. When it’s in your brain, the consequences are deadly.

Last week, a team of NIH-funded researchers based at the Baylor College of Medicine in Texas and at the University of Minnesota revealed a clever way to identify genes that normally increase the levels of these rogue disease-causing proteins.


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