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Prof. Debbie Toiber <\/p>\n
(Photo: Hertzel Yosef)<\/p>\n
\u201cWe can\u2019t prevent this damage because it happens naturally, but we may be able to repair it better and stop the domino effect before disease develops.\u201d<\/p>\n
How do you do that?
\n\u201cI focus on neurodegenerative diseases such as Alzheimer\u2019s and Parkinson\u2019s. Only about 5% of Alzheimer\u2019s cases are genetic; the other 95%, risk rises with age and reaches about one in three among people 80 and older.<\/p>\n
\u201cWe\u2019re trying to understand what it is about aging that leads to disease, what goes wrong along the way and how to detect that disruption early. We identify trajectories, which are decision points where a cell \u2018chooses\u2019 whether to head toward pathological aging or healthy aging. If we detect that early, we may be able to protect the cell and steer it in a healthier, more resilient direction.\u201d<\/p>\n
What tools do you use for the study?
\n\u201cWe use chemical reactions in animal models such as worms, flies and mice, as well as in human cells. We have technology that allows us to take a skin cell from a specific person, turn it into a stem cell and then grow, for example, neurons from it to study what happens in the brain.<\/p>\n
\u201cTo avoid waiting decades, we use models of cells and animals that can\u2019t properly repair DNA damage. In mice, for example, the damage accumulates so quickly that within three weeks they appear old and develop diseases similar to Alzheimer\u2019s.<\/p>\n
\u201cIn one experiment, we received a cellular sample from a family in which both parents carried a defect in the same DNA repair gene. The parents were unaffected, but children who inherited both faulty copies lived up to age 2. That suggests there is a threshold for how much damage the body can absorb while remaining healthy.\u201d<\/p>\n
Does the gene responsible for repair change over time?
\n\u201cYes. Early on, we produce millions of copies of it. It repairs damage effectively, but not perfectly. Every day, each cell in our body sustains between 1,000 and 1 million new injuries, and the gene can\u2019t fix them all. As we live longer, the unrepaired damage accumulates. At the same time, levels of the gene decline. We don\u2019t know exactly why, but it likely becomes \u2018exhausted\u2019 due to stress signals.\u201d<\/p>\n
Can\u2019t it be duplicated?
\n\u201cWhen an extra copy is added (as shown in research by Prof. Haim Cohen), mice lived about 10% longer. But to add more, you\u2019d need to reach every cell in the body, and there are millions. Instead of duplicating it, we want to find ways to activate it so it works harder, even if there\u2019s less of it.\u201d<\/p>\n
What happens when cells malfunction?
\n\u201cCells that aren\u2019t functioning properly can self-destruct to avoid becoming diseased. Cancer, for example, is an age-related disease, and these altruistic cells may self-destruct to prevent becoming cancerous. That may sound good, but if too many cells die, the brain shrinks and we lose tissue. <\/p>\n
“Another option is that they become \u2018senescent\u2019 cells, while doing half the work and disrupting their neighboring tissues by sending inflammatory signals. In our research, we try to prevent cells from reaching those states.\u201d<\/p>\n
Can we prevent this damage?
\n\u201cWe have control over some factors. Studies consistently show that good muscle mass, a diet without processed foods, strong social and family support and sufficient sleep all contribute to healthier aging. We know that a sedentary lifestyle and processed foods increase the risk of accelerated aging. In one experiment, we fed high-fat food to mice with a defect in a DNA repair gene. Their cognitive decline was much worse compared to mice that ate a healthy diet. So even if we don\u2019t know whether our genes are impaired, we can still help ourselves by adopting a healthy lifestyle.\u201d<\/p>\n
Do you manage to follow that lifestyle?
\n\u201cI try to stay active. I always have.\u201d<\/p>\n
I suggest you take a group of mice, expose them to sirens every three hours and check their aging after three weeks. It\u2019s reasonable to assume the mental stress we all live with accelerates aging.
\n\u201cWe know stress causes accelerated aging and may result in deteriorating more quickly across many measures, but I believe it\u2019s reversible and can be repaired.<\/p>\n
\u201cWe\u2019ve recently begun research on PTSD. We\u2019re trying to understand what happens at the molecular level to propose interventions that can prevent that decline.\u201d<\/p>\n
What would be a breakthrough for you?
\n\u201cIdentifying the point at which a cell decides whether to move toward disease or remain healthy and then finding a way to push it toward the healthy path.\u201d<\/p>\n
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