Blood analysis may reveal Alzheimer’s risk
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A blood test might one day predict a person’s risk of developing dementia, a new study suggests. It links certain levels of two proteins in blood samples with a 10-fold increase of developing Alzheimer’s disease and other forms of dementia.
Alzheimer’s disease has no known cure, and its causes are also mysterious. The disease typically progresses over years, gradually robbing elderly patients of memory, language and other crucial mental skills. In very rare cases, people in their 30s or 40s can develop “early-onset Alzheimer’s”.
Notably, those who carry the genetic mutations known to encourage early-onset Alzheimer’s have elevated levels of certain protein fragments, called amyloid fragments, in their blood.
This finding caught the attention of epidemiologist Monique Breteler of Erasmus Medical Centre in Rotterdam, The Netherlands, because the same amyloid fragments form plaques in the brains of patients with Alzheimer’s, regardless of the age at which they develop the disease.
Dementia watch
Breteler and colleagues studied how blood levels of two slightly different amyloid fragments – Beta 1-40 and the slightly longer Beta 1-42 – relate to the risk of dementia among people who do not have early-onset Alzheimer’s.
The team took blood samples from 6713 volunteers over the age of 55 years who showed no signs of dementia. They analysed the blood for levels of the two amyloid fragments, and monitored the cognitive function of 1756 volunteers randomly selected from the sample group over an average of 8.6 years.
Of the closely monitored subgroup, 9% developed dementia. While most of these developed Alzheimer’s, others had dementia relating to other illnesses, such as Parkinson’s disease. To strengthen their analysis, researchers also included data from 230 patients in the initial study group who developed dementia, such as Alzheimer’s.
Dangerous ratio
The study showed that those with the highest Beta 1-40 levels combined with the lowest Beta 1-42 levels were 10 times more likely to develop dementia as those who had the lowest amounts of both fragment types. Subjects with high levels of both amyloid Beta 1-40 and amyloid Beta 1-42 had about the same risk of developing dementia as those with low levels of both.
As a result, Breteler believes it is the ratio of these amyloid fragments that matters. She speculates that lower levels of amyloid Beta 1-42 – the predominant component of Alzheimer’s plaques in the brain – may indicate that this is getting deposited in the brain instead of circulating in the body. Previous studies have suggested that amyloid Beta 1-40 is deposited in plaques during the later stages of Alzheimer’s.
But Breteler admits that it remains “debatable” how much protein levels in the blood reflect those in the brain.
While she says that this is by far the largest study to see how well the ratio of these amyloid fragments in the blood predict dementia, she also cautions that it is too soon to consider the method a reliable test. “I don’t think that we are at a test yet,” she stresses. “I think that’s really the next step.”
Alzheimer’s disease has no known cure, and its causes are also mysterious. The disease typically progresses over years, gradually robbing elderly patients of memory, language and other crucial mental skills. In very rare cases, people in their 30s or 40s can develop “early-onset Alzheimer’s”.
Notably, those who carry the genetic mutations known to encourage early-onset Alzheimer’s have elevated levels of certain protein fragments, called amyloid fragments, in their blood.
This finding caught the attention of epidemiologist Monique Breteler of Erasmus Medical Centre in Rotterdam, The Netherlands, because the same amyloid fragments form plaques in the brains of patients with Alzheimer’s, regardless of the age at which they develop the disease.
Dementia watch
Breteler and colleagues studied how blood levels of two slightly different amyloid fragments – Beta 1-40 and the slightly longer Beta 1-42 – relate to the risk of dementia among people who do not have early-onset Alzheimer’s.
The team took blood samples from 6713 volunteers over the age of 55 years who showed no signs of dementia. They analysed the blood for levels of the two amyloid fragments, and monitored the cognitive function of 1756 volunteers randomly selected from the sample group over an average of 8.6 years.
Of the closely monitored subgroup, 9% developed dementia. While most of these developed Alzheimer’s, others had dementia relating to other illnesses, such as Parkinson’s disease. To strengthen their analysis, researchers also included data from 230 patients in the initial study group who developed dementia, such as Alzheimer’s.
Dangerous ratio
The study showed that those with the highest Beta 1-40 levels combined with the lowest Beta 1-42 levels were 10 times more likely to develop dementia as those who had the lowest amounts of both fragment types. Subjects with high levels of both amyloid Beta 1-40 and amyloid Beta 1-42 had about the same risk of developing dementia as those with low levels of both.
As a result, Breteler believes it is the ratio of these amyloid fragments that matters. She speculates that lower levels of amyloid Beta 1-42 – the predominant component of Alzheimer’s plaques in the brain – may indicate that this is getting deposited in the brain instead of circulating in the body. Previous studies have suggested that amyloid Beta 1-40 is deposited in plaques during the later stages of Alzheimer’s.
But Breteler admits that it remains “debatable” how much protein levels in the blood reflect those in the brain.
While she says that this is by far the largest study to see how well the ratio of these amyloid fragments in the blood predict dementia, she also cautions that it is too soon to consider the method a reliable test. “I don’t think that we are at a test yet,” she stresses. “I think that’s really the next step.”
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