The struggle to maintain a healthy weight is a lifelong challenge for many of us. In fact, the average American packs on an extra 30 pounds from early adulthood to age 50. What’s responsible for this tendency toward middle-age spread? For most of us, too many calories and too little exercise definitely play a role. But now comes word that another reason may lie in a strong—and previously unknown—biochemical mechanism related to the normal aging process.
My 8-year-old nephew Luke has a sixth-grade reading level, while still in the third grade. Yet, he often struggles to finish his chores. He carries a timer in his backpack to keep himself on task. His school provides Luke with special assistance, including extra time for tests and repeated, detailed instruction. The challenges arise because Luke, like his mother Rebecca, has attention-deficit/hyperactivity disorder (ADHD).
Isaac was born to fight. Arriving more than five weeks early by emergency C-section, it wasn’t just his way of coming into the world that made him different from his three brothers. While he initially looked healthy, his parents soon realized Isaac’s health was something he and the entire family would need to be fighting for every single day.
For gene therapy research, the perennial challenge has been devising a reliable way to insert safely a working copy of a gene into relevant cells that can take over for a faulty one. But with the recent discovery of powerful gene editing tools, the landscape of opportunity is starting to change. Instead of threading the needle through the cell membrane with a bulky gene, researchers are starting to design ways to apply these tools in the nucleus—to edit out the disease-causing error in a gene and allow it to work correctly.
In a new study of families affected by Attention Deficit Hyperactivity Disorder (ADHD), National Institutes of Health (NIH) Intramural researchers have identified different connections in the brain that children may inherit from their parents and are linked to the disorder.
Dr. Hong Xu's team’s expertise in mitochondrial DNA genetics, along with a strong mitochondrial biology research group in the IRP, allowed them to solve the fundamental biological question of how organisms are able to stop the accumulation of mitochondrial DNA mutations from being passed on to future generations.
Given that Alzheimer’s is such a complex disease with many causes and pathways, it is not surprising that the search for effective treatments has proven difficult. So I spoke with Drs. Yujun Hou and Hyundong Song, postdoctoral fellows in the IRP’s Laboratory of Molecular Gerontology at the National Institute on Aging (NIA) to learn more about their approaches to meeting the challenge.
Hi, my name is James. I’ve always really liked science and I want to be a scientist when I grow up, but I never got to see where scientists work until I went to Take Your Child to Work Day at NIH with my Auntie Kit. It was awesome!
Are you beginning to think that slide rules look alike? If you could see the types and number of scales, you’d understand that each slide rule model is different. There are specialized scales for cubes, spheres, voltage, etc. Check out a few of the slide rules that made history with IRP investigators.
As an “I Am Intramural” Blog reader, you likely know that the IRP is comprised of more than 6,000 scientists conducting basic, translational, and clinical research in more than 50 buildings on six different IRP campuses around the U.S.But, do you know the answers to the questions in the following IRP Pop Quiz?
Researchers at the NIH IRP have access to:
a) Laboratory equipment sales, rental, repairs, and maintenance
b) Plants and marine organisms for research
c) High-throughput DNA sequencing
d) A and C
e) All of the above