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WEDNESDAY, July 17, 2019 (HealthDay News) – One of the hallmarks of Alzheimer's disease is the accumulation of beta-amyloid plaques in the brain, but the role these plaques play in the development of the disease remains unclear.
Researchers have now taken the first steps to monitor the progression of plaque accumulation in patients still alive. This way of "staging" the disease has implications for research and one day may help doctors treat this debilitating and fatal disease.
"It is possible to determine the progress of beta amyloid deposition by means of PET," said lead researcher Niklas Mattsson, an badociate professor of clinical neuroscience at the University of Toronto. University of Lund, Sweden.
When beta-amyloid appears, it follows certain steps, he explained. Some areas of the brain are involved early, others in the middle stage and others in the advanced stage of Alzheimer 's.
These stages are also badociated with other features of Alzheimer's disease, such as tau levels [another type of protein] in cerebrospinal fluid, cognitive decline and brain dieback, "Mattsson added.
"This staging system can be used both to improve research and perhaps also in the context of clinical trials, to determine if certain drugs are likely to be more effective at certain stages of the disease. of Alzheimer's, "said Mattsson.
By the time Alzheimer's disease is generally diagnosed, the brain is already destroyed, said Meredith Braskie, an badistant professor of neurology at the University of Southern California in Los Angeles. She was not involved in the study.
The disease takes years to develop, which is why it is important to find a way to diagnose it quickly, said Braskie. Most plaque studies have been done on the brains of deceased people.
"This study is important because it looked at how amyloid spreads in living patients and proposes steps for that," Braskie said.
Although no curative treatment exists for Alzheimer's disease today, this discovery could also help test drugs as they develop, she said. declared.
But, "it's not directly related to patient care," Braskie said. "It's more for research to see if the treatments work."
For the study, Mattsson and his colleagues used PET scans from the Alzheimer's Disease Neuroimaging Initiative database. Of the 741 participants, 304 had no cognitive impairment, 384 had mild cognitive impairment, and 53 had Alzheimer's disease. Patients were followed at two, four and six years of age.
At the beginning of the study, about 98% of the 2,072 scans had not been performed. About 15% of people in the early stages of plaque development are likely to progress to a more advanced stage, as are 71% of stage 1 and 53% stage 2.
When patients switched from Stage 1 to Stage 2 and Stage 3, the researchers noted that amyloid plaque was developing in more vital areas of the brain.
Interestingly, researchers found that nearly 1% of patients returned to a lower stage. The higher stages were related to higher concentrations of tau in the cerebrospinal fluid. More tau at stage 2 indicated a faster progression of cognitive decline. The researchers were able to confirm their findings in a different group of 474 patients.
The affected brain areas differed at each stage and were also related to differences in genetics, blood circulation, brain cell behavior, and cholesterol levels.
"I think it's clear from these data that earlier the diagnosis of Alzheimer's disease is corroborated by amyloid imaging, it is likely that clinicians initiate drug therapy," he said. Dr. Sam Gandy. He is Chair of Alzheimer's Disease Research and Director of the Mount Sinai Center for Cognitive Health and NFL Neurological Care in New York.
This would be a change from the current practice of not starting drug treatment until patients have pbaded the mild cognitive deficit and are not affected by Alzheimer's disease, Gandy said. did not participate in this study.
However, Gandy is not sure that early drug treatment early in a mild cognitive impairment and that a scan shows that plaque would be beneficial to all or some patients.
In addition, he would like to see if the staging system would work the same way in patients with and without mutations in the APOE gene, which are linked to Alzheimer's disease.
"These data could potentially have an impact on the care and design of future research studies," Gandy said. "If these changes in practice would have significant benefits for patients, it's not clear."
The report was published online July 17 in the journal JAMA Neurology, to coincide with a presentation of the results at the annual meeting of the Alzheimer's Association, Los Angeles.
More information
To learn more about Alzheimer's disease, go to the Alzheimer's Association.
SOURCES: Niklas Mattsson, M.D., Ph.D., Associate Professor, Clinical Neuroscience, University of Lund, Sweden; Sam Gandy, M.D., Ph.D., Professor, Neurology and Psychiatry, Chair of Alzheimer's Disease Research, Director of Mount Sinai Center for Cognitive Health and Neurological Care NFL, New York; Meredith Braskie, Ph.D., Assistant Professor, Neurology, University of Southern California, Keck School of Medicine, Los Angeles; July 17, 2019, JAMA Neurologyonline
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