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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 RSSNew 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.
Mobile microscopes illuminate the brain
The majority of our life is spent moving around a static world and we generate our impression of the world using visual and other senses simultaneously.
This is your brain on fatty acids
Saturated fats have a deservedly bad reputation, but Johns Hopkins scientists have discovered that a sticky lipid occurring naturally at high levels in the brain may help us memorize grandma's recipe for cinnamon buns, as well as recall how, decades ago, she served them up steaming from the oven.
Sight gone, but not necessarily lost?
Like all tissues in the body, the eye needs a healthy blood supply to function properly. Poorly developed blood vessels can lead to visual impairment or even blindness.
Widely used cholesterol-lowering drug may prevent progression
Simvastatin, a commonly used, cholesterol-lowering drug, may prevent Parkinson's disease from progressing further. Neurological researchers at Rush University Medical Center conducted a study examining the use of the FDA-approved medication in mice with Parkinson's disease and found that the drug successfully reverses the biochemical, cellular and anatomical changes caused by the disease.
Statins show dramatic drug and cell dependent effects in the brain
Besides their tremendous value in treating high cholesterol and lowering the risk of heart disease, statins have also been reported to potentially lower the risks of other diseases, such as dementia.
Researchers find brain cell transplants help repair neural damage
A Swiss research team has found that using an animal's own brain cells (autologous transplant) to replace degenerated neurons in select brain areas of donor primates with simulated but asymptomatic Parkinson's disease and previously in a motor cortex lesion model, provides a degree of brain protection and may be useful in repairing brain lesions and restoring function.
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