A team led by researchers at the Banner Good Samaritan Medical Center in Phoenix scanned the brains of 12 young patients who have a mutation of the APOE gene associated with a high risk of Alzheimer's disease. They found that the young patients shared some of the same metabolic changes seen in patients with advanced and mild cases of the disease.
"People with this susceptibility gene have reduced brain activity in each of the brain regions that are progressively affected later in life" among Alzheimer's patients, said Dr. Eric M. Reiman, chief of the Positron Emission Tomography Center at Banner and first author of the study.
The study appears this week in the Proceedings of the National Academy of Sciences.
Reiman said researchers have yet to prove a link between the metabolic changes and the development of the disease, but the finding "suggests that there are brain changes many years before the possible onset of memory and thinking problems.
"We believe these brain changes provide a foothold for the development of some of the microscopic and metabolic abnormality that we see in patients later in life," he said.
Bill Thies, vice president of Medical and Scientific Affairs for the Alzheimer's Association, said the Reiman study is part of an ongoing effort by many researchers to find a way to identify at an early age who will later develop the memory loss and thinking problems of Alzheimer's disease.
There is no proven preventive therapy now for Alzheimer's, but Thies said that when the therapy is found, doctors will need to have tests that can identify patients.
Thies said studies of the way the brain processes glucose in patients with Alzheimer's is considered quite promising in the search for early clinical evidence of the disease.
"The best that can be said is that there is a correlation between glucose utilization and (Alzheimer's) pathology," said Thies. "Whether it is causative, we can't say."
Alzheimer's is a progressive and fatal brain disease that slowly wipes out memory and, eventually, all cognitive function. The disease is marked by deposits of plaques and tangles in key parts of the brain, causing the progressive and wholesale death of neurons. The precise cause is unknown and there is no cure, although some drugs can modify the course of the disease in some patients.
In the study, Reiman and his team conducted brain scans on 12 patients with a gene mutation linked to Alzheimer's. They compared these scans with those from 15 patients who were not carriers of the gene. All the study subjects were between 20 and 39, an age which is usually decades before the onset of Alzheimer's symptoms.
Reiman said they found that the gene carriers had an abnormally low level of brain glucose metabolism, when compared to the non-carriers. He said the low level of metabolism occurred in the same sections of the brain that other studies have shown are most dramatically affected in Alzheimer's patients. Earlier studies have found low levels of glucose metabolism in the brains of patients with mild and severe Alzheimer's.
"This study suggests that it may be possible to target brain changes and prevent Alzheimer's by intervening at a young time when that intervention will be particularly effective," said Reiman. "The thinking is that the earlier you can detect brain changes, the earlier you might be able to intervene with a prevention therapy."
By Paul Recer