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New step in DNA damage response in neurons discovered
January 20, 2009Researchers have identified a biochemical switch required for nerve cells to respond to DNA damage.
The finding, scheduled for advance online publication in Nature Cell Biology, illuminates a connection between proteins involved in neurodegenerative disease and in cells' response to DNA damage.
Most children with the inherited disease ataxia telangiectasia are wheelchair-bound by age 10 because of neurological problems. Patients also have weakened immune systems and more frequent leukemias, and are more sensitive to radiation.
The underlying problem comes from mutations in the ATM (ataxia telangiectasia mutated) gene, which encodes an enzyme that controls cells' response to and repair of DNA damage.
ATM can be turned on experimentally by treating cells with chemicals that damage DNA. After other proteins in the cell detected broken DNA needing repair, scientists had thought that the ATM protein could activate itself directly. Emory researchers have shown that an additional step is necessary first.
"In neurons that are not dividing anymore, we now know that another regulator is involved: Cdk5," says Zixu Mao, MD, PhD, associate professor of pharmacology and neurology at Emory University School of Medicine.
Working with postdoctoral fellows Bo Tian, PhD and Qian Yang, PhD, Mao found that the Cdk5 protein must activate ATM before ATM can do its job in neurons.
The results support the idea that Cdk5 may be a potential drug target. Cdk5 contributes to normal brain development, and aberrant Cdk5 activity is known to be involved in the death of neurons in several neurodegenerative diseases, including Alzheimer's, Parkinson's and amyotrophic lateral sclerosis.
"Cdk5 has a complex character," Mao says. "It can be bad for neurons if its activity is either too high or too low."
Mao says he and his colleagues were intrigued by reports that in these diseases, neurons that had stopped dividing appear to restart that process, copying their DNA, before dying.
"That's what really kicked us into high gear," he says.
The same process, called "mitotic catastrophe," occurs when neurons suffer DNA damage. Inhibiting either Cdk5 or ATM can reduce the number of neurons that suffer mitotic catastrophe after DNA damage, the authors found.
Emory University
The underlying problem comes from mutations in the ATM (ataxia telangiectasia mutated) gene, which encodes an enzyme that controls cells' response to and repair of DNA damage.
ATM can be turned on experimentally by treating cells with chemicals that damage DNA. After other proteins in the cell detected broken DNA needing repair, scientists had thought that the ATM protein could activate itself directly. Emory researchers have shown that an additional step is necessary first.
"In neurons that are not dividing anymore, we now know that another regulator is involved: Cdk5," says Zixu Mao, MD, PhD, associate professor of pharmacology and neurology at Emory University School of Medicine.
Working with postdoctoral fellows Bo Tian, PhD and Qian Yang, PhD, Mao found that the Cdk5 protein must activate ATM before ATM can do its job in neurons.
The results support the idea that Cdk5 may be a potential drug target. Cdk5 contributes to normal brain development, and aberrant Cdk5 activity is known to be involved in the death of neurons in several neurodegenerative diseases, including Alzheimer's, Parkinson's and amyotrophic lateral sclerosis.
"Cdk5 has a complex character," Mao says. "It can be bad for neurons if its activity is either too high or too low."
Mao says he and his colleagues were intrigued by reports that in these diseases, neurons that had stopped dividing appear to restart that process, copying their DNA, before dying.
"That's what really kicked us into high gear," he says.
The same process, called "mitotic catastrophe," occurs when neurons suffer DNA damage. Inhibiting either Cdk5 or ATM can reduce the number of neurons that suffer mitotic catastrophe after DNA damage, the authors found.
Emory University
Neurons Current Events and Neurons News RSSScripps research scientists find new link between insulin and core body temperature
A team led by scientists at The Scripps Research Institute have discovered a direct link between insulin-a hormone long associated with metabolism and metabolic disorders such as diabetes-and core body temperature.
New Down syndrome treatment suggested by Stanford/Packard study in mice
At birth, children with Down syndrome aren't developmentally delayed. But as they age, these kids fall behind. Memory deficits inherent in Down syndrome hinder learning, making it hard for the brain to collect experiences needed for normal cognitive development.
Cognitive dysfunction reversed in mouse model of Down syndrome
A study by neuroscientist William C. Mobley, MD, PhD, chair of the Department of Neurosciences at the University of California, San Diego School of Medicine, and colleagues at Stanford University Medical School has demonstrated a possible new approach to slowing the inevitable progression of cognitive decline found in Down's syndrome.
Pushing the brain to find new pathways
Until recently, scientists believed that, following a stroke, a patient had about six months to regain any lost function. After that, patients would be forced to compensate for the lost function by focusing on their remaining abilities.
Scientists decipher the formation of lasting memories
Researchers at Karolinska Institutet have discovered a mechanism that controls the brain's ability to create lasting memories. In experiments on genetically manipulated mice, they were able to switch on and off the animals' ability to form lasting memories by adding a substance to their drinking water.
Developmental delay could stem from nicotinic receptor deletion
The loss of a gene through deletion of genetic material on chromosome 15 is associated with significant abnormalities in learning and behavior, said a consortium of researchers led by Baylor College of Medicine (www.bcm.edu) in a report that appears online today in the journal Nature Genetics.
New TMS clinic offers noninvasive treatment for major depression
Rush University Medical Center has opened the Transcranial Magnetic Stimulation (TMS) Clinic to offer patients suffering from major depression a safe, effective, non-drug treatment.
Researchers explore new ways to prevent spinal cord damage using a vitamin B3 precursor
Substances naturally produced by the human body may one day help prevent paralysis following a spinal cord injury, according to researchers at Weill Cornell Medical College. A recent $2.5 million grant from the New York State Spinal Cord Injury Research Board will fund their research investigating this possibility.
Estrogen therapy likely must be given soon after menopause to provide stroke protection
For estrogen replacement to provide stroke protection, it likely must be given soon after levels drop because of menopause or surgical removal of the ovaries, scientists report in the Journal of Neuroscience.
Researchers identify drug candidate for treating spinal muscular atrophy
A chemical cousin of the common antibiotic tetracycline might be useful in treating spinal muscular atrophy (SMA), a currently incurable disease that is the leading genetic cause of death in infants.
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