Alzheimer’s Disease Study Finds Possible Genetic Clue
By John E. Carey
Peace and Freedom
January 15, 2007
Medical experts from the Center for Research in Neurodegenerative Diseases at the University of Toronto, Columbia University Medical Center in New York, Boston University Medical Center, the Mayo Clinic College of Medicine in Jacksonville, Florida, and other research centers have completed a five year study on Alzheimer’s disease.
The doctors have concluded that a new gene they have identified apparently can raise the risk of developing the most common form of Alzheimer’s disease.
Alzheimer’s disease is an incurable brain disorder that is the top cause of dementia in the elderly.
Up to 4.5 million Americans are estimated to have Alzheimer's, which gradually destroys memory and other mental abilities. No cure has been found.
The number of Americans with Alzheimer’s will greatly expand as “baby bomber” reach their elderly years, adding a huge financial burden to those paying for elderly care.
The most common variant of the disease, “late onset Alzheimer’s,” inflicts people over the age of 65. About 90 percent of all Alzheimer’s cases are “late onset.” The rarer early-onset is found less often in people from about age 30 to 65.
The doctors reported their findings in the journal Nature Genetics on Sunday.
The genetic indicator discovered in the research is being called SORL1.
People from four ethnic groups: Caribbean-Hispanics, North Europeans, black Americans and Israeli-Arabs were involved in the study. Doctors said they found certain variations of SORL1 more often in people with late-onset Alzheimer's disease than in healthy people.
For several years, many scientists have believed that Alzheimer's begins with the buildup in the brain of a gooey material called amyloid that form plaques in the brain. These plaques at first slow normal cognitive action and eventually disrupt it altogether. The material stems from a protein called amyloid precursor protein, or APP.
SORL1, doctors now believe, controls the distribution of APP inside nerve cells of the brain.
When working normally, the gene prevents APP from being degraded into a toxic byproduct called amyloid beta peptide. When SORL1 is deficient, it allows more of the bad amyloid beta peptide to accumulate, fostering amyloid plaques.
People who inherit certain variations of the SORL1 gene appear to have an increased risk of getting Alzheimer's after age 60.
“Our study says that changes in the SORL1 gene might be a cause of the disease," said Dr. Richard Mayeux at the Columbia University Medical Center.
Alzheimer's is a complex disease that gradually destroys a person's memory, ability to learn, reasoning, ability to make judgments, communication skills and the ability to carry out normal daily activities. Scientists have struggled to understand the biology of the disease and its root causes.
"It's another clue to the way in which this disease comes about, another piece of the puzzle," said Dr. Peter St. George-Hyslop, director of the Center for Research in Neurodegenerative Diseases at the University of Toronto.
"Every time you get a piece of the puzzle and you can relate it to something else in the puzzle, you're that much closer to knowing what the picture on the puzzle is," he added.
Dr. St. George-Hyslop said it is premature to say what percentage of cases of late-onset Alzheimer's disease can be attributed to SORL1. ApoE4, which also may be involved in the production of amyloid plaques, has been linked to about 20 percent of late-onset Alzheimer's cases.
"This appears to be the fifth Alzheimer's disease gene, and there are likely to be other important genetic variants that need to be identified before the entire picture is complete," Dr. Richard Mayeux of Columbia University Medical Center in New York, also involved in the research, said in a statement.
If the findings of this study are confirmed by other scientists, it would be "a very substantial step forward in our understanding of the genetics of Alzheimer's disease," said Jonathan Haines of Vanderbilt University.
By shedding light on the biology of the illness, the discovery could help lead scientists to find new treatments, he and other experts said.
Sam Gandy, a spokesman for the Chicago-based Alzheimer's Association said if the results of this study are confirmed it may be possible to one day develop a blood test to identify people who are “at risk” for late onset Alzheimer’s.
But the test would just offer a risk profile and couldn't predict who would actually get the disease, he says.
More and more doctors and researchers are now convinced that late-onset Alzheimer's is not triggered by a single gene and is probably influenced by many factors, including lifestyle and diet, says Gandy, who is the director of the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia.
Peace and Freedom
January 15, 2007
Medical experts from the Center for Research in Neurodegenerative Diseases at the University of Toronto, Columbia University Medical Center in New York, Boston University Medical Center, the Mayo Clinic College of Medicine in Jacksonville, Florida, and other research centers have completed a five year study on Alzheimer’s disease.
The doctors have concluded that a new gene they have identified apparently can raise the risk of developing the most common form of Alzheimer’s disease.
Alzheimer’s disease is an incurable brain disorder that is the top cause of dementia in the elderly.
Up to 4.5 million Americans are estimated to have Alzheimer's, which gradually destroys memory and other mental abilities. No cure has been found.
The number of Americans with Alzheimer’s will greatly expand as “baby bomber” reach their elderly years, adding a huge financial burden to those paying for elderly care.
The most common variant of the disease, “late onset Alzheimer’s,” inflicts people over the age of 65. About 90 percent of all Alzheimer’s cases are “late onset.” The rarer early-onset is found less often in people from about age 30 to 65.
The doctors reported their findings in the journal Nature Genetics on Sunday.
The genetic indicator discovered in the research is being called SORL1.
People from four ethnic groups: Caribbean-Hispanics, North Europeans, black Americans and Israeli-Arabs were involved in the study. Doctors said they found certain variations of SORL1 more often in people with late-onset Alzheimer's disease than in healthy people.
For several years, many scientists have believed that Alzheimer's begins with the buildup in the brain of a gooey material called amyloid that form plaques in the brain. These plaques at first slow normal cognitive action and eventually disrupt it altogether. The material stems from a protein called amyloid precursor protein, or APP.
SORL1, doctors now believe, controls the distribution of APP inside nerve cells of the brain.
When working normally, the gene prevents APP from being degraded into a toxic byproduct called amyloid beta peptide. When SORL1 is deficient, it allows more of the bad amyloid beta peptide to accumulate, fostering amyloid plaques.
People who inherit certain variations of the SORL1 gene appear to have an increased risk of getting Alzheimer's after age 60.
“Our study says that changes in the SORL1 gene might be a cause of the disease," said Dr. Richard Mayeux at the Columbia University Medical Center.
Alzheimer's is a complex disease that gradually destroys a person's memory, ability to learn, reasoning, ability to make judgments, communication skills and the ability to carry out normal daily activities. Scientists have struggled to understand the biology of the disease and its root causes.
"It's another clue to the way in which this disease comes about, another piece of the puzzle," said Dr. Peter St. George-Hyslop, director of the Center for Research in Neurodegenerative Diseases at the University of Toronto.
"Every time you get a piece of the puzzle and you can relate it to something else in the puzzle, you're that much closer to knowing what the picture on the puzzle is," he added.
Dr. St. George-Hyslop said it is premature to say what percentage of cases of late-onset Alzheimer's disease can be attributed to SORL1. ApoE4, which also may be involved in the production of amyloid plaques, has been linked to about 20 percent of late-onset Alzheimer's cases.
"This appears to be the fifth Alzheimer's disease gene, and there are likely to be other important genetic variants that need to be identified before the entire picture is complete," Dr. Richard Mayeux of Columbia University Medical Center in New York, also involved in the research, said in a statement.
If the findings of this study are confirmed by other scientists, it would be "a very substantial step forward in our understanding of the genetics of Alzheimer's disease," said Jonathan Haines of Vanderbilt University.
By shedding light on the biology of the illness, the discovery could help lead scientists to find new treatments, he and other experts said.
Sam Gandy, a spokesman for the Chicago-based Alzheimer's Association said if the results of this study are confirmed it may be possible to one day develop a blood test to identify people who are “at risk” for late onset Alzheimer’s.
But the test would just offer a risk profile and couldn't predict who would actually get the disease, he says.
More and more doctors and researchers are now convinced that late-onset Alzheimer's is not triggered by a single gene and is probably influenced by many factors, including lifestyle and diet, says Gandy, who is the director of the Farber Institute for Neurosciences at Thomas Jefferson University in Philadelphia.
posted by John Carey at 8:03 AM
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