11-08-2009, 06:39 AM
Children fathered by older men have an increased risk of schizophrenia in later life, possibly because of mutations in their father’s DNA, according to a new study from Sweden.
A link between paternal age and schizophrenia has been reported before but scientists were not sure whether this was due to increasing mutations with advancing age or the result of inherited personality traits.
To find out, researchers at the University of Wales College of Medicine in Cardiff and Gothenburg University in Sweden examined the medical records of 50,087 Swedish army conscripts recruited between 1969 and 1970.
Their findings, reported in the British Journal of Psychiatry, show that 362 of the former soldiers had been diagnosed with schizophrenia by 1996.
Their fathers’ ages varied between 19 and 65. In a control group of men without schizophrenia, the fathers’ ages ranged from 15 to 75.
The study found that the odds of developing schizophrenia increased by 30 percent for each 10-year increase in paternal age.
Adjusting for poor social integration had only a minimal effect on the findings, suggesting personality traits were not a major factor.
“This supports the hypothesis that accumulating germ cell mutations may lead to an increase in genetic liability to schizophrenia in the offspring,” Dr Stanley Zammit, from the University of Wales, said.
Extra copies of gene may cause Parkinson’s: Certain patients with Parkinson’s disease carry extra copies of a gene that may clog their brains with excess proteins — a finding that may lead to better treatments and perhaps a way to stop the disease, scientists said.
They found members of a family plagued by Parkinson’s carried additional copies of a gene called alpha synuclein. A buildup of the protein the gene controls is believed to cause the Parkinson’s symptoms.
The findings, reported in Friday’s issue of the journal Science, might shed light on all cases of Parkinson’s and perhaps other brain diseases, the researchers said.
The four patients each have not only an extra copy of the gene, but also of an entire region of the chromosome that carries it, said Andrew Singleton of the National Institute on Aging’s Laboratory of Neurogenetics, who led the study.
“It’s amazingly rare,” Singelton said in a telephone interview. “It includes 16 other genes that flank synuclein.”
His team is now checking whether these patients have extra high levels of the protein synuclein, controlled by the gene, as suggested by other studies of Parkinson’s patients.
“This study is an exciting step forward in our understanding of this disease,” Singelton said.
“It contributes to the growing body of evidence suggesting that genetic variations in alpha-synuclein contribute to Parkinson’s disease. It suggests that in Parkinson’s disease, both mutated and normal alpha-synuclein behave in a way that is quantitatively different from the way the protein functions in people without Parkinson’s disease.”
Parkinson’s is the second most common neurodegenerative disease after Alzheimer’s. Incurable and always fatal, Parkinson’s affects an estimated 500,000 Americans. It is caused by the death of brain cells that produce dopamine, a neurotransmitter or message-carrying chemical important to muscle movement. Patients develop tremors and gradually become paralyzed.
Singleton and colleagues were studying the “Iowa kindred,” a family in which many relatives developed Parkinson’s or related neurological diseases at an average age of 34. They found four family members had two extra versions of the gene.
“We hope that this type of basic research will yield new understandings that will ultimately allow us to go beyond just treating the symptoms of Parkinson’s disease to one day halting the disease’s progression,” said Matthew Farrer of the Mayo Clinic in Rochester, Minnesota, who worked on the study.
The symptoms in this family are similar to those in other Parkinson’s patients, the researchers noted. Insights into many diseases have been provided by families carrying a rare genetic mutation that points doctors in the right direction for finding broader causes of illness.
They could also help in other diseases, such as Alzheimer’s disease in Down syndrome patients. Down syndrome is caused by an extra copy of chromosome 21, which in turn causes overproduction of certain proteins.
Cambridge, Massachusetts-based Alnylam Pharmaceuticals said it had signed an agreement with the Mayo Clinic to try to develop a drug that will work against the synuclein gene.
Alnylam was founded by biotechnology researchers seeking to start a new field of drug research called RNA interference. The idea is to interfere with the output of faulty genes.
http://www.thenews.com.pk/daily_detail.asp?id=207341
A link between paternal age and schizophrenia has been reported before but scientists were not sure whether this was due to increasing mutations with advancing age or the result of inherited personality traits.
To find out, researchers at the University of Wales College of Medicine in Cardiff and Gothenburg University in Sweden examined the medical records of 50,087 Swedish army conscripts recruited between 1969 and 1970.
Their findings, reported in the British Journal of Psychiatry, show that 362 of the former soldiers had been diagnosed with schizophrenia by 1996.
Their fathers’ ages varied between 19 and 65. In a control group of men without schizophrenia, the fathers’ ages ranged from 15 to 75.
The study found that the odds of developing schizophrenia increased by 30 percent for each 10-year increase in paternal age.
Adjusting for poor social integration had only a minimal effect on the findings, suggesting personality traits were not a major factor.
“This supports the hypothesis that accumulating germ cell mutations may lead to an increase in genetic liability to schizophrenia in the offspring,” Dr Stanley Zammit, from the University of Wales, said.
Extra copies of gene may cause Parkinson’s: Certain patients with Parkinson’s disease carry extra copies of a gene that may clog their brains with excess proteins — a finding that may lead to better treatments and perhaps a way to stop the disease, scientists said.
They found members of a family plagued by Parkinson’s carried additional copies of a gene called alpha synuclein. A buildup of the protein the gene controls is believed to cause the Parkinson’s symptoms.
The findings, reported in Friday’s issue of the journal Science, might shed light on all cases of Parkinson’s and perhaps other brain diseases, the researchers said.
The four patients each have not only an extra copy of the gene, but also of an entire region of the chromosome that carries it, said Andrew Singleton of the National Institute on Aging’s Laboratory of Neurogenetics, who led the study.
“It’s amazingly rare,” Singelton said in a telephone interview. “It includes 16 other genes that flank synuclein.”
His team is now checking whether these patients have extra high levels of the protein synuclein, controlled by the gene, as suggested by other studies of Parkinson’s patients.
“This study is an exciting step forward in our understanding of this disease,” Singelton said.
“It contributes to the growing body of evidence suggesting that genetic variations in alpha-synuclein contribute to Parkinson’s disease. It suggests that in Parkinson’s disease, both mutated and normal alpha-synuclein behave in a way that is quantitatively different from the way the protein functions in people without Parkinson’s disease.”
Parkinson’s is the second most common neurodegenerative disease after Alzheimer’s. Incurable and always fatal, Parkinson’s affects an estimated 500,000 Americans. It is caused by the death of brain cells that produce dopamine, a neurotransmitter or message-carrying chemical important to muscle movement. Patients develop tremors and gradually become paralyzed.
Singleton and colleagues were studying the “Iowa kindred,” a family in which many relatives developed Parkinson’s or related neurological diseases at an average age of 34. They found four family members had two extra versions of the gene.
“We hope that this type of basic research will yield new understandings that will ultimately allow us to go beyond just treating the symptoms of Parkinson’s disease to one day halting the disease’s progression,” said Matthew Farrer of the Mayo Clinic in Rochester, Minnesota, who worked on the study.
The symptoms in this family are similar to those in other Parkinson’s patients, the researchers noted. Insights into many diseases have been provided by families carrying a rare genetic mutation that points doctors in the right direction for finding broader causes of illness.
They could also help in other diseases, such as Alzheimer’s disease in Down syndrome patients. Down syndrome is caused by an extra copy of chromosome 21, which in turn causes overproduction of certain proteins.
Cambridge, Massachusetts-based Alnylam Pharmaceuticals said it had signed an agreement with the Mayo Clinic to try to develop a drug that will work against the synuclein gene.
Alnylam was founded by biotechnology researchers seeking to start a new field of drug research called RNA interference. The idea is to interfere with the output of faulty genes.
http://www.thenews.com.pk/daily_detail.asp?id=207341