Alzheimer’s disease initially and simultaneously affects different regions of the brain, and contrary to what was thought, it does not start from a single area from which a chain reaction starts. It has been seen by an international team, led by the
University of Cambridge.
These findings could have important implications for the development of possible treatments, they have been published in the journal
«Science Advances», and open new ways of understanding the progress of this disease and other neurodegenerative pathologies, and new ways of developing future treatments.
The researchers used five different data sets, which when combined and applied to the same mathematical model, allowed them to observe that the mechanism that controls the rate of
progression in Alzheimer’s is the replication of aggregates in individual regions of the brain, and not the aggregate propagation from one region to another.
For many years, the processes within the brain that lead to Alzheimer’s disease have been described using terms such as “Cascade” and “chain reaction”. It is a difficult disease to study, as it develops over decades, and a definitive diagnosis can only be made until after examining samples of brain tissue after death.
Previously, studies were largely based on animal models and concluded that Alzheimer’s disease spread rapidly, as clumps of toxic proteins colonized different parts of the brain.
“Alzheimer’s was thought to develop in a similar way to many cancers: aggregates form in one region and then spread throughout the brain,” says Georg Meisl of the
Cambridge Department of Chemistry, first author of the article.
“Instead, we found that when the disease begins, there are already aggregates, in multiple regions of the brain, so trying to stop the spread between regions will do little to stop the disease,” Meisl adds.
“It is exciting to see progress in this field: fifteen years ago, we and others, determined the basic molecular mechanisms in laboratories; but now we can study this process at the molecular levelr in real patients, which is an important step to someday develop treatments, “says Professor Tuomas Knowles, also from the Department of Chemistry.
Researchers have found that replication of Tau aggregates is slow, taking up to five years.
“Neurons are incredibly effective at stopping the formation of aggregates, but we need to find ways to improve even more if we want to find an effective treatment,” warns David Klenerman of the UK Dementia Research Institute on the
University of Cambridge. “It’s fascinating how biology has evolved to stop protein aggregation.”
“The key finding is that stopping the replication of aggregates instead of their spread, it will be more effective in the stages of the disease that we study “, details Knowles.
George is Digismak’s reported cum editor with 13 years of experience in Journalism