Alzheimer's disease (AD) is the most common neurodegenerative disease, with more than 40 million cases reported worldwide. AD is characterized by the aggregation of both the β-Amyloid (Aβ) proteins into plaques and of the tau proteins into neurofibrillary tangles (NFTs) known collectively as aggregates which cause brain cells to die and the brain to shrink.

It had been believed that aggregation begins in a single location, spreading from one brain region to the next. A key limiting factor in disease progression is at what rate these processes occur and how important the local replication of seeds and their spread over longer length scales between brain regions, are for determining the time scale of human disease. 

Recent results, reported in the journal Science Advances, have opened up new avenues of understanding the progress of Alzheimer's and other neurodegenerative diseases and possibly new ways that future treatments might be developed.

The researchers developed a mathematical model to simulate the progression of the disease and applied it to five different imaging datasets. By combining the five different datasets, the researchers observed that the mechanism controlling the rate of progression in Alzheimer's disease is the replication of aggregates in individual regions of the brain and not the spread of aggregates from one region to another.