We all know what aging means but do we understand what it means to grow old? And can we slow it down? Our ongoing coverage from SfN.

It’s a cliché to say some of us will age gracefully, but the fact remains that a few rare individuals will run marathons in their 80s, while a significantly larger percentage will lose their memory. Wouldn’t it be great to bottle the biological makeups of all those future healthy, functioning octogenarians so we all could increase our chances of living a healthy life, or at least keeping the aging demons at bay a little longer.

The challenge for aging researchers is identifying the mechanisms that cause us to age. We know that age is the biggest risk factor for Alzheimer’s, diabetes, cancer, osteoporosis and many other chronic diseases. Bu we are less clear about the cellular events that cause our bodies to start to wear down r and we don’t know how to measure or model this cascade of events in a way that helps lead us to a new generation of “aging therapeutics”.

“If you get a meeting of aging biologists and ask them to define aging it typically causes an argument that results in something like ‘bad things happen and then you die,’ ” said biologist Brian Kennedy during a panel on aging therapeutics that coincided with the Society for Neuroscience meeting in San Diego this week.

Kennedy, a researcher with the Buck Institute for Research on Aging, has been studying animal models of aging for over two decades. He says misfolding proteins, adult stem cell dysfunction, inflammation and other drivers of aging are planted well before we develop diabetes, Alzheimer’s, cancer and other diseases that increase with age.  

“Depending upon which direction you go in will drive different chronic diseases of aging,” says Kennedy. “If it’s a protein folding change it can be neurodegenerative, if it’s metabolic changes it can be diabetes.”

Kennedy was among a panel of experts who gathered Monday in San Diego to discuss how to establish disease indications of aging and model aging to accelerate translational research. The luncheon was sponsored by Charles River. The other panelists included: Kimberly Scearce-Levie, Head of Preclinical Translational Biology at Denali Therapeutics, Barbara Tate, a Partner with the Dementia Discovery Fund, Eliezer Masliah, National Institute on Aging’s Division of Neuroscience and Robert Hodgson, Director, Science R&D, Charles River. The discussion was moderated by Steven Braithwaite, Chief Scientific Officer at Alkahest.

 Here are some other highlights of the meeting.

  • A pill to treat aging? There are about 74 million Baby Boomers worldwide (me included) who would love to delay aging. Tate, who is also a neuroscientist, said if you could find a pill to delay aging, and therefore prevent or delay the onset of diseases that now gobble up so much of our health care spending, the win would be huge. According to Kennedy, it might not be as hard as we think. Kennedy said finding a gene or drug that treats aging is considered a longshot, but in animals, at least, it’s actually pretty easy to find genetic mutations to extend life span. And Kennedy also thinks that we are, in a way, already treating aging with drugs that lower cholesterol or control blood sugar.  
  • Should we delay aging?  Masliah from the NIA said someone approached him recently during an NIH meeting questioning the economic value of delaying aging, given the huge cost involved in treating age-related disorders later in life. Masliah also wonders if we are confusing normal aging with the pathological aging that occurs when diseases like Alzheimer’s take hold. “I don’t think necessarily that what we call aging is abnormal or something we need to fight against or find a therapeutic for,” said Masliah. But Kennedy countered that with about a quarter of the world population over the age of 60, it actually makes more sense to delay aging given the shortage of working class people needed to fill their shoes. The reason for extending life span is not so they can retire and have more time to spend on the golf course people, it is because you are going to allow people to be functional longer and work longer and promote economic growth longer, he said.
  • Why don’t mice age like humans? A phenomenon that continues to confound Scearce-Levie is modeling age in mice. Scearce-Levie says when one sees an older individuals who is physically active, mentally fit, and socially engaged the assumption is that the person must have really good genes. Yet when you raise mice in environmentally identical setting, some of the mice still go on to develop cataracts, tumors and cognitive deficits while others appear perfectly normal. Independent of the models we set up and the genetic manipulations we make, says Scearce-Levie, how can we drill down to understand the subtle shift in the homeostatic network that is determining which mice line up just fine for 2-3 years and which ones end up with tumors?
  • The Funding Picture: Drug discovery carries all kinds of risks that developers must weigh. Tate predicts that private investors will eventually want to support biotherapeutic s for aging. “Venture is drawn to where the demographics are driving us and there is no way we are going to ignore 20-25% of the population,” she said.

 

How to Cite:

McEnery, Regina.McEnery, Regina. Is It Possible To Treat Aging. Eureka blog. Nov. 17, 2016. http://eureka.criver.com/is-it-possible-to-treat-aging/