Caption: A stylized image of the MC4R-expressing neurons (in red) within the brain’s PVH, which is the “heart of hunger” Credit: Michael Krashes, NIDDK, NIH
If you’ve ever skipped meals for a whole day or gone on a strict, low-calorie diet, you know just how powerful the feeling of hunger can be. Your stomach may growl and rumble, but, ultimately, it’s your brain that signals when to start eating—and when to stop. So, learning more about the brain’s complex role in controlling appetite is crucial to efforts to develop better ways of helping the millions of Americans afflicted with obesity .
Thanks to recent technological advances that make it possible to study the brain’s complex circuitry in real-time, a team of NIH-funded researchers recently made some important progress in understanding the neural basis for appetite. In a study published in the journal Nature Neuroscience, the researchers used a variety of innovative techniques to control activity in the brains of living mice, and identified one particular circuit that appears to switch hunger off and on .
Time for another LabTV video! Today, I’d like you to meet Melissa Young, a third-year graduate student in the College of Pharmacy, University of Georgia, Athens. Young, who is doing research in the lab of James Franklin, says her scientific goal is to help build the scientific case that oxidative stress plays a key role in Alzheimer’s disease.
Young also has a personal reason for wanting to her research to succeed. From her experiences with a beloved grandmother and aunt, she has seen first-hand the heartbreaking effects of Alzheimer’s disease and other forms of dementia on both patients and their loved ones. Currently, there is no cure for Alzheimer’s disease and no treatments to halt or reverse its progression. That’s one of the reasons why Young has chosen to go into an area of science focused on translating basic discoveries into new therapeutics.
Study after study has found no link between autism spectrum disorders (ASD) and the measles-mumps-rubella (MMR) vaccine—or any vaccine for that matter. Yet many parents still refuse or delay vaccinations for their young children based on misplaced fear of ASD, which can be traced back to a small 1998 study that’s since been debunked and retracted . Such decisions can have a major negative impact on public health. With vaccination rates in decline, we’ve recently seen the resurgence of measles and other potentially fatal childhood infectious diseases.
Among the parents most likely to avoid getting their kids vaccinated are those who already have a child with ASD. So, it’s especially important and timely news that researchers have once again found no link between MMR vaccines and ASD—even among children known to be at greater risk for autism because an older sibling has the developmental brain disorder.
While attending college in her native Colombia, Yakeel T. Quiroz joined the Grupo de Neurociencias de Antioquia. This dedicated group of Colombian researchers, healthcare workers, and students has worked for many years with a large extended family in the northwestern district of Antioquia that is truly unique. About half of the more than 5,000 family members inherit a gene mutation that predisposes them to what is known locally as “la bobera,” or “the foolishness,” a devastating form of early-onset Alzheimer’s disease. Those born with the mutation are cognitively healthy through their 20s, become forgetful in their 30s, and descend into full-blown Alzheimer’s disease by their mid-to- late 40s. Making matters worse, multiple family members sometimes are in different stages of dementia at the same time, including the caregiver attempting to hold the household together.
Quiroz, now a researcher at Massachusetts General Hospital in Boston, vowed never to forget these families. She hasn’t, working hard to understand early-onset Alzheimer’s disease and helping to establish the Forget Me Not Initiative to raise money for affected families. With an NIH Director’s Early Independence Award, Quiroz also recently launched her own lab to pursue an even broader scientific opportunity: discover subtle pre-symptomatic changes in the brain years before they give rise to detectable Alzheimer’s. What she learns will have application not only to detect and possibly treat early-onset Alzheimer’s in Colombia but also to understand the late-onset forms of the dementia that affect an estimated 35.6 million people worldwide.
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 , 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 , 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.