A new Harvard study adds fuel to the debate over the role amyloid plaques in the brain play in causing Alzheimer’s.
All AD patients have amyloid plaques in their brains, but so do many elderly people who don’t get Alzheimer’s. This runs counter to the theory that amyloid plaques cause or play a role in the disease.
So, now Harvard researchers report that otherwise healthy people with plaques also “also had structural changes similar to but less pronounced than the neurodegenerative changes” that are seen in those with AD.
In other words, even though the people have no symptoms, the link between plaques and neurodegeneration suggests they might be on the road to Alzheimers, according to the Harvard news office story.
“Our findings support the theory that Alzheimer’s disease begins many years before symptoms appear and that amyloid plaque is an early sign of this process,” says Keith Johnson of Massachusetts General Hospital (MGH) Imaging, senior author of the study. “We see that when amyloid deposits are present, even in cognitively normal individuals, the degenerative changes of Alzheimer’s are under way. Long-term studies to track these changes and observe how they evolve are ongoing.”
For the other side of the amyloid argument, it is useful to go back to the debate that flared up of the use of PET scans to the diagnosis of AD. In a NYTimes op-ed Sanjay W. Pimplikar of the Cleveland Clinic’s wrote:
First, about the diagnostic tests: A PET scan detects clumps of a deformed protein called amyloid beta, commonly known as plaques. The presence of these plaques has been a gold standard of Alzheimer’s pathology since 1906, when Dr. Alois Alzheimer first identified them in a patient.
However, we now know that roughly one-third of all elderly adults have such plaques in their brains yet function normally. And eleven clinical trials, recently made public by a group of drug companies, that were aimed at reducing these plaques in Alzheimer’s patients all failed to show cognitive improvement, even when the brains were cleared of plaques.
Thus, the presence of plaques cannot predict with any accuracy or specificity that an individual is going to acquire the disease — and researchers are increasingly looking beyond the amyloid hypothesis for an adequate explanation for Alzheimer’s.