(Reuters) – People with a family history of Alzheimer’s disease often have clumps of a toxic protein in their brains even though they are perfectly healthy, researchers said on Monday.
They said the findings could lead to new ways to identify people most likely to develop Alzheimer’s disease, when there is still time to do something about it.
“The hope is to one day be able to diagnose very clearly the Alzheimer’s disease process before any symptoms occur, when the brain is still healthy. Then the treatments would have the best chance of success,” said Lisa Moscone of New York University Langone Medical Center, whose study appears in the Proceedings of the National Academy of Sciences.
The team wants to continue to follow the people in the study to see whether they develop dementia, and they want to replicate the findings in a much larger study.
Several teams have been working on better ways to detect early-stage Alzheimer’s disease in hopes of developing drugs that can fight it before it causes too much damage.
Current treatments cannot reverse the course of Alzheimer’s, a mind-robbing form of dementia that affects more than 26 million people globally.
Moscone’s team used an imaging technique called positron emission tomography or PET with a fluorescent dye called Pittsburgh Compound B that lights up clumps of a protein called beta amyloid that are a hallmark of Alzheimer’s disease.
The team imaged the brains of 42 people with an average age of 65, all with healthy brain function. Of these, 14 people had mothers who had Alzheimer’s; 14 had fathers with the disease; and 14 had parents with healthy brain function.
Brain scans of all 42 showed that those whose parents — either fathers or mothers — had Alzheimer’s were more likely to have amyloid plaques in their brains.
This was especially true of people whose mothers had Alzheimer’s.
ScienceDaily (Jan. 13, 2010) — A study published in the January 13, 2010 issue of the Journal of Neuroscience links a loss of smell function in Alzheimer’s disease (AD) model animals with amyloid (protein) accumulation in the brain, a distinguishing hallmark of Alzheimer’s disease. Research conducted by NYU Langone Medical Center suggests that olfactory dysfunction, a common symptom of AD, may serve as an early diagnostic tool for the disease.
After researchers tried to reduce levels of two enzymes, beta secretase and gamma secretase, simultaneously in mice they found this combination approach worked better and prevented some of the negative side effects of treating just one of the enzymes that produces the amyloid plaque found in Alzheimer’s disease. Read More…
In examining the hippocampus, the region of the brain that controls memory, diffusion tensor imaging (DTI), an MRI technique that measures the random motion of water in tissue, better predicts verbal and spatial memory performance in healthy people than conventional MRI techniques that measure the volume of the hippocampus. Read More…
Heavy smokers and drinkers develop Alzheimer’s years before people who don’t drink or smoke as much, a new report says.
The study, presented Wednesday at the American Academy of Neurology meeting in Chicago, suggests heavy drinking and smoking might be accelerating damage to the brain, which could lead to Alzheimer’s.
ut the flip side of the study is a message of hope: People who cut back or stop habits such as excessive smoking or drinking might reduce their risk of developing Alzheimer’s at a younger age. Instead of struggling with forgetfulness at age 59, such people might delay symptoms until age 65 or 70, says researcher Ranjan Duara of the Mount Sinai Medical Center in Miami Beach.
Duara and his colleagues examined 938 people ages 60 and older with a diagnosis of Alzheimer’s, a disease that causes confusion, memory loss and behavioral problems. The team asked family members to provide patients’ histories of drinking and smoking. Then the team identified patients who had APOE4, a gene that increases the risk of developing Alzheimer’s late in life.
For people with a common genetic variation, researchers have discovered signs of the possible onset of Alzheimer’s before a patient would be clinically diagnosed by a doctor.
In people with the ApoE4 gene variation, one previously implicated as affecting the likelihood of Alzheimer’s, researchers have been able to pinpoint some signs of memory loss beginning in the person’s mid- to late-50s — without the patient having full-blown Alzheimer’s disease or dementia.
“[One could argue] we really captured for the first time the onset of Alzheimer’s disease,” explained Dr. Richard Caselli, a neurologist at the Mayo Clinic in Scottsdale, Ariz.
“What’s passing as normal aging itself correlates with the most common genetic risk factor for Alzheimer’s disease,” he said, adding that the symptoms are noticeable in a clinical setting, but not in everyday life.
“It’s not the sort of thing that you can look at somebody or they can look at themselves and know.”
Researchers caution that when in interpreting the findings, one should keep in mind that people who had shown some memory loss were still functioning normally and having the gene did not impair anyone at an earlier age.