BAR HARBOR Scientists at the MDI Biological Laboratory have published research which improves the understanding of the mechanisms by which the lifespan of roundworms can be lengthened by cutting back on calories.

It has been known for decades that drastically restricting certain nutrients without causing malnutrition prolongs health and lifespan in a wide range of species, but the molecular mechanisms underlying this effect have remained a mystery.

In a paper recently published in the journal Aging Cell, MDI Biological Laboratory scientist Aric Rogers shed light on an important genetic pathway underlying this process, raising the possibility that therapies can be developed that prolong the healthy years without having to suffer the consequences of a severely restricted diet.

Aric Rogers. PHOTO COURTESY OF THE MDI BIOLOGICAL LABORATORY

Its tantalizing to think that we might be able to activate a protective response to enhance our own health without resorting to extreme dietary regimes, Rogers said.

Rogers studies mechanisms important to the positive effects of dietary restriction in an intact organism the tiny roundworm, C. elegans as opposed to cells in a petri dish. This roundworm is an important model in aging research because it shares nearly half of its genes with humans and because of its short lifespan it lives for only two to three weeks which allows scientists to study many generations over a short period of time.

Arics identification of a molecular mechanism governing the life-prolonging effects of dietary restriction is a validation of our unique approach to research in aging and regenerative biology, said Kevin Strange, president of the laboratory. Our use of whole organisms as research models provides greater insight into the many factors controlling physiological processes than the use of cells alone.

The life-prolonging effects of dietary restriction, or calorie restriction, occur in just about every animal tested. They are thought to be an evolutionary adaptation to harsh environmental conditions. In the absence of enough food to eat, evolution has programmed organisms to switch from a growth mode to a survival mode so they can live long enough to reproduce when conditions improve.

The identification of a mechanism underlying the protective effect of dietary restriction could lead to therapies for age-related diseases, including Alzheimers and Parkinsons, that are associated with diminished cellular quality control. Alzheimers, for instance, is associated with the build-up of the toxic protein beta amyloid in the brain, and Parkinsons with a build-up of a toxic protein called alpha synuclein.

The link between aging and weakened cellular housekeeping functions raises the possibility that new drugs to prolong lifespan also could delay the onset of age-related degenerative diseases. Now that Rogers has identified a link, the next step is to investigate cause and effect by manipulating the genetic pathways that inhibit protein formation to see if the bodys ability to clear molecular clutter is improved.

We think therapies to activate these protective pathways could not only prolong lifespan but also delay the onset of age-related diseases, Rogers said. Most older people suffer from multiple chronic diseases. Anti-aging procedures applied to disease models almost always delay disease onset and improve outcomes, which suggests that disease-suppressing benefits may be accessed to extend healthy human lifespan.

The MDI Biological Laboratory, located in Bar Harbor, is an independent, nonprofit biomedical research institution focused on increasing healthy lifespan and increasing our natural ability to repair and regenerate tissues damaged by injury or disease. The institution develops solutions to complex human health problems through research, education and ventures that transform discoveries into cures. Visit mdibl.org.

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