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Scientists Prevent Brain-Cell Suicide to Keep Birds Singing
By Alexis Madrigal July 09, 2008 | 3:59:14 PMCategories: Biology
Some birds, caged or not, only sing when they really need to, namely, during the breeding season. After it's over, their musical neurons die-off, and they are left tune-less.
But now, scientists at the University of Washington have shown they can keep the birds singing, temporarily, by stopping the action of an enzyme key to their brains' natural cell-death processes. As cell-death mechanisms are similar across species, the research could open up new avenues of research on degenerative and age-related diseases like Alzheimer's.
Programmed cell death, or apoptosis, is common in multicellular organisms and aids important biological processes, like maintaining homeostasis and acting as the chisel in skeletal development. While there are many reasons that a cell could sense it is supposed to die, the actual suicide process is generally the same: A group of enzymes called caspases execute on the order for cellular degeneration.
What the researchers have shown in work to be published tomorrow in the Journal of Neuroscience is that inhibiting the caspases preserves neurons and brain-region function; in this case, singing.
"In the future, physicians might be able to stabilize people who have suffered a stroke using these inhibitors," said Eliot Brenowitz, a University of Washington professor of psychology and zoology, in a release.
The study itself involved 15 male white-crowned sparrows, like the one seen in the picture above. After the birds were captured in the wild, the researchers simulated breeding-season lighting conditions and gave the birds steroids to boost their song-control regions. Then the steroids were cut and the birds were returned to nonbreeding light. The control group of birds showed cell death in the song-control region, but those given the caspase-inhibiting hormone retained their signing neurons.
One caveat though: The researchers euthanized the birds after one, three and seven days, so they wouldn't know how long the caspase inhibitors would work for.
Still, for a neurodegenerative disorder located in a specific region of the brain, like some types of ataxia, Brenowitz's research could represent a promising new clinical avenue.
"We don't yet know all the ways in which hormones prevent brain cell death, but this study shows that hormones block caspases and so preserve neurons," said Brenowitz.
Image: Tsu Wei Wang, courtesy the University of Washington
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The life of Marie Schlau, a German Jewish girl born in 1833 hides great unsolved mysteries: accidents, disappearances, enigmas, unknown diagnoses, disturbing murders, love, tenderness, greed, lies, death ... alternatively a different story unfolds every time and takes us closer to the present. Thus, there are two parallel stories unravelling, each in a different age and place, which surprisingly converge in a revelatory chapter.
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Currently, BabelFAmily is financing two promising research projects aimed at finding a cure for Friedreich's Ataxia. Whenever you make a donation to us or purchase a copy of "The legacy of Marie Schlau", this is where all funds raised will be devoted to:
1) Gene Therapy for Friedreich's Ataxia research project:
The project is the result of an initiative of Spanish people affected by this rare disease who are grouped in GENEFA in collaboration with the Spanish Federation of Ataxias and the BabelFAmily. The Friedreich’s Ataxia Research Alliance (FARA), one of the main patients’ associations in the United States now joins the endeavour.
2) Frataxin delivery research project:
The associations of patients and families Babel Family and the Asociación Granadina de la Ataxia de Friedreich (ASOGAF) channel 80,000 euros of their donations (50% from each organisation) into a new 18-month project at the Institute for Research in Biomedicine (IRB Barcelona). The project specifically aims to complete a step necessary in order to move towards a future frataxin replacement therapy for the brain, where the reduction of this protein causes the most damage in patients with Friedreich’s Ataxia.
The study is headed by Ernest Giralt, head of the Peptides and Proteins Lab, who has many years of experience and is a recognised expert in peptide chemistry and new systems of through which to delivery drugs to the brain, such as peptide shuttles—molecules that have the capacity to carry the drug across the barrier that surrounds and protects the brain. Since the lab started its relation with these patients’ associations in 2013*, it has been developing another two projects into Friedrich’s Ataxia.