Swedish researchers have found that inflammatory changes in the brain can be spotted almost two decades before an Alzheimer's patient shows their first symptoms. This could potentially provide a window for patients to make lifestyle changes to prepare for its onset, or for early prophylactic or modifying treatment to slow down or stop the progress of the disease, when such therapies eventually become available.

"This study increases our understanding of the early stages of Alzheimer's disease," Agneta Nordberg, a professor at Karolinska and co-author of the study, published in Brain, told daily newspaper Dagens Nyheter.

"There has been a huge focus on amyloids in Alzheimer's research, but it has not been so successful in treatment trials, perhaps because most studies have been conducted in patients with already pronounced symptoms. This discovery shows that there are other components that are important enough to explore," she noted.

The team looked at members of families with four different known Alzheimer’s mutations and a group of patients with non-inherited, "sporadic" Alzheimer’s disease. Memory tests and PET scans were used. Tracer molecules PIB, Deprenyl and FDG were employed to determine amyloid plaque levels and inflammatory changes, specifically astrocyte activation. The scans were repeated on half of the nearly 50 individuals in the study after three years to check for changes.

“Inflammatory changes in the form of higher levels of brain astrocytes are thought to be a very early indicator of disease onset,” noted Nordberg, a professor at the Department of Neurobiology, Care Sciences and Society, Center for Alzheimer Research at Karolinska.

“Astrocyte activation peaks roughly twenty years before the expected symptoms and then goes into decline, in contrast to the accumulation of amyloid plaques, which increases constantly over time until clinical symptoms show. The accumulation of amyloid plaque and the increase in number of astrocytes therefore display opposing patterns along the timeline.”

The study suggests that targeting this early inflammation might even stop amyloid plaques from developing in the first place.

“As of today, no therapeutic strategy has succeeded at changing the course of the disease,” first author Dr. Elena Rodriguez-Vieitez told The Telegraph.

“The current therapies are only symptomatic, that is, they mitigate symptoms but they don’t change the course of the disease. So an early diagnosis today would not help prevent dementia using the currently available drugs.

“Our research aims at understanding especially the earliest phases of the disease. Clinical trials aimed at clearing amyloid plaques have not yet succeeded at curing the disease, and therefore it is necessary to find new therapeutic targets.”

These latest findings come on the heels of 2015 reports by researchers at University College London that Alzheimer's "seeds" of dementia could possibly be transmitted, similar to Creuzfeldt Jakob Disease, between people accidentally, via blood transfusion or other bodily substances, such as growth hormone.

"The seeds will potentially stick to metal surfaces whatever the instrument is. With prions, we know quite a lot about that. Certainly, there are potential risks with dentistry where it's impacting on nervous tissue, for example root canal treatments," said Professor John Collinge, director of the Medical Research Council Prion Unit at University College London, according to the paper.

"If you are speculating that amyloid beta seeds might be transferred by instruments, one would have to consider whether certain types of dental procedures might be relevant."

Although the risk is low, the researchers said that checking such transmission routes should be a research priority.

But it is not "contagious" in any way, such as the flu. "You can't catch it by living with someone who has Alzheimer's disease or being a carer," he stressed to the Telegraph. "No-one should consider cancelling or delaying any kind of surgery. But I think it would be prudent to do some research in this area."