Author: Robert O'Brien

Dogs, Dwarfism and Aging: Lessons From IGF1

The really fun thing about discussing signaling networks (the inputs that let cells make decisions based on their environment) in aging is the wide range of ways that these pathways exert their influence. See my previous blog on myostatin for an example of this. Cells are like a computer—they take inputs (nutrition, hormones, toxic molecules) and use their existing programming (epigenetic state) to make decisions. Components that control one process, such as regulating body size, can play roles in completely different processes. Today, I’ll discuss an example involving Insulin-like growth factor 1 or IGF1, a close relative of Insulin...

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Bacterial Defense Systems Provide New Tools to Treat Human Diseases

Bacterial enzymes have played an important role in modern biotechnology and molecular biology through their ability to manipulate complicated molecules like DNA. In the late 1960’s and early 1970’s, scientists studying how bacteria defend themselves from viruses identified proteins called restriction enzymes that cut specific sequences of viral DNA and prevent viruses from infecting and killing bacteria. This discovery was the basis for the Nobel Prize in medicine in 1978. Shortly afterward in the 1980’s, a molecule from a different type of bacteria that lives in hot springs was used as a tool to amplify pieces of DNA (a...

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Amyloid-beta and Alzheimer’s disease

AD is defined by the presence of “amyloid plaques” (sticky globs of a protein fragment called amyloid beta or Aβ) in the brains of people with dementia. There is lots of good evidence that Aβ can cause AD. For example, there are families that inherit early-onset forms of AD, and have mutations in the protein itself or in enzymes that process the protein into sticky fragment forms.

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Sarcopenia, myostatin, and Belgian blue bulls

Inspired by Matt Laye’s excellent blog on sarcopenia, the loss of muscle mass during aging, I’ve decided to write a follow up blog about unusual cases that have taught scientists about the mechanisms behind muscle loss and how to prevent it. This is not the first article written on the subject, so please read more here, here and here. Our story begins with a breed of cows that was identified in Belgium in 1808. These cows displayed an unusually muscular appearance, and in the years since, have been used for both dairy and meat. It was discovered that this...

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Weekly SAGE 12/1/14: Understanding the normal function of Huntington Disease gene

By Rob O’Brien Huntington’s disease (HD) is a genetic disorder that affects roughly 1 in 10,000 Americans. While the genetic basis of the disease was identified in 1993, there are still gaps in our understanding of what the protein that causes the disease (called, appropriately, Huntingtin) does in healthy people. The protein is ubiquitous (it is present in all of the tissues of the body) and is essential (meaning that mice without the protein do not survive). Last week, researchers at UC Irvine published results showing that there is a portion of the huntingtin protein not associated with the disease that can physically stick to some fragments of the protein that is associated with the disease. This newly characterized portion of the protein seems to be important for the process of autophagy (literally “self-eating”), a process by which cells get rid of damaged organelles and proteins and which is known to be important for healthy aging. So why is this exciting? Sticky aggregates of the huntingtin protein can be removed by two processes: autophagy and via the proteasome. Autophagy is disrupted in neurodegenerative diseases in general, and Huntington’s disease specifically. So what does this mean for neurodegenerative disorders of aging? Well, this new function of a protein implicated in a major neurodegenerative disease may give us clues about what is going wrong in this disease, as well as others...

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