Scientists identify how Alzheimer’s progresses in the brain

Hope that discovery can lead to development of new treatments

The diseases affects an estimated 44 million people worldwide (Getty)

Scientists have identified what drives the progression of Alzheimer’s within the brain, raising hope that new treatments could be to developed to target the disease.

Rather than spreading like a cancer from a single source, toxic clumps of protein slowly accumulate in multiple areas of the brain at the same time, researchers from the University of Cambridge found.

Forming over a number of years, these clusters – known as aggregates – cause cells to die and the brain to shrink, resulting in memory loss, personality changes and difficulty carrying out daily functions.

The research, published in the journal Science Advances, shows that the rate of progression in Alzheimer’s disease is shaped by the replication of aggregates in individual regions of the brain, and not the spread of aggregates from one region to another.

How quickly these clusters then kill the brain’s cells determines the overall speed of deterioration in brain functioning.

Two types of protein – called tau and amyloid-beta – clump together to form the aggregates. The scientists used post-mortem brain samples, as well as scans from living patients, including those with mild cognitive impairment and those with late-stage disease, to track the aggregation of tau.

They found that the replication of tau aggregates is surprisingly slow – taking up to five years.

“Neurons are surprisingly good at stopping aggregates from forming, but we need to find ways to make them even better if we’re going to develop an effective treatment,” said co-author Professor Sir David Klenerman, from the UK Dementia Research Institute at the University of Cambridge.

The researchers say their findings could be used to help the development of treatments for Alzheimer’s disease, which affects an estimated 44 million people worldwide, by targeting the most important processes that occur when humans develop the disease.

“The key discovery is that stopping the replication of aggregates rather than their propagation is going to be more effective at the stages of the disease that we studied,” said co-senior author Professor Tuomas Knowles, from Cambridge’s Yusuf Hamied Department of Chemistry.

The researchers are now planning to look at the earlier processes in the development of Alzheimer’s, and extend the studies to other brain diseases where the replication of tau aggregates plays a key role in progressing the condition.

Commenting on the study, Dr Sara Imarisio, head of research at Alzheimer’s Research UK, said: “Hopefully this study and others like it will help focus the development of future treatments that target tau, so any future treatments have a better chance of slowing the disease processes themselves and have benefit for people with dementia.”