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In the human body, cells are constantly making life-or-death decisions. If they make the wrong choice, the result can be cancer, infection or even Alzheimer's. NPR's Jon Hamilton reports on efforts to treat diseases by influencing the process known as programmed cell death.
JON HAMILTON, BYLINE: In Alzheimer's, brain cells die too soon. Cancer cells don't die soon enough. That's because both diseases alter the way cells decide when to end their lives. Doug Green, of St. Jude Children's Research Hospital in Memphis, has spent much of his career studying this process.
DOUG GREEN: Cell death sounds like sort of a morbid thing to work on, but in fact it's really essential for our health.
HAMILTON: Green says coaxing nerve cells to live longer could help people with Alzheimer's, Parkinson's or ALS. Getting tumor cells to die sooner could help with other diseases.
GREEN: If we can specifically modify or modulate the tendency of a cell to die, then of course we have the potential to treat a cancer.
HAMILTON: So many scientists are looking to control programmed cell death. One of them is Randal Halfmann at the Stowers Institute for Medical Research in Kansas City, Missouri. He's been studying immune cells that self-destruct when they come in contact with molecules that present a threat to the body.
RANDAL HALFMANN: They have to somehow recognize that in this vast array of other complex molecules and then within minutes kill themselves.
HAMILTON: Like a soldier diving on a grenade. Halfmann's team focused on special proteins inside cells that can initiate this process.
HALFMANN: And what was surprising is that the proteins that are involved, when they recognize that virus, they implode.
HAMILTON: Instantly crumpling and linking up with similarly affected proteins to form what's known as a death fold polymer. That starts a chain reaction, creating more death fold polymers, which ultimately kills the cell. This process takes a burst of energy, and Halfmann's team couldn't locate the source. Then they thought about reusable handwarmers, which produce heat by changing from a liquid to a crystallized solid.
HALFMANN: There's a little button inside. You can click it, and then it will crystallize right in front of you, and that releases all this energy. And that's exactly what we envision what's happening for these proteins.
HAMILTON: Halfmann found it a bit unsettling to think that so many cells carry these self-destruct buttons just waiting to be pushed.
HALFMANN: You know, it just seemed like a really terrible way to live - right? - every moment of a cell's life, to be at risk of spontaneously dying.
HAMILTON: Of course, death is what you want for a cancerous cell or one that's infected with a virus. But Halfmann thinks this hair-trigger system might be needlessly killing brain cells in diseases like Alzheimer's. He notes that one hallmark of Alzheimer's is a misfolded protein called amyloid.
HALFMANN: That amyloid, for reasons we don't really understand, ends up killing the neurons, and in some cases, it will go on and kill other neurons.
HAMILTON: Perhaps because those misfolded amyloid proteins, much like death fold proteins, seem to replicate and form crystal-like structures. So Halfmann has begun looking for ways to keep brain cells alive by making it harder for those crystals to form. Doug Green, the researcher in Memphis, says biotech firms are trying to halt the process at a different point, by blocking the communication pathways involved in cell death.
GREEN: One of these pathways is a major target for many pharmaceutical companies that are working furiously to come up with a way to block that particular death fold interaction.
HAMILTON: Green says the companies are betting on products known as antisense drugs, which can prevent a cell from making key proteins involved in Alzheimer's and other neurodegenerative diseases.
GREEN: If they're right - I think they are - it's going to cure a lot of diseases, diseases that we associate with aging and inflammation.
HAMILTON: In part, by changing how cells make life-or-death decisions.
Jon Hamilton, NPR News. Transcript provided by NPR, Copyright NPR.
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