Cause of Alzheimer's disease progression in the brain discovered
Steph Deschamps / October 30, 2021
Clusters of toxic proteins, thought to be responsible for the cognitive decline associated with Alzheimer's disease, reach different areas of the brain and accumulate there over decades, according to a new study published Friday.
The paper, published in Science Advances, is the first to use human data to quantify the speed of molecular processes leading to this neurodegenerative disease, and could influence how treatments are designed.
It also overturns the theory that clusters form in a single location and trigger a chain reaction in other areas, a pattern seen in mice. Such spread can occur, but is not the primary driver, the researchers say.
Two things made this work possible, Georg Meisl, a chemist at the University of Cambridge and one of the lead authors of the paper, told AFP.
First, the study of very detailed data from PET scans (a type of medical imaging test, nldr) and various datasets collected, and the mathematical models that have been developed over the last 10 years.
The researchers used 400 brain samples taken after the death of people with Alzheimer's and 100 PET scans taken of people living with the disease to track tau protein aggregation.
Amyloid and another protein called beta-amyloid build up, causing brain cells to die and the brain to shrink.
This causes memory loss and an inability to perform daily tasks. The disease is a major public health problem, affecting more than 40 million people worldwide.
The researchers also found that it takes five years for the aggregates to double in number. This is an encouraging figure, according to Georg Meisl, because it shows that neurons are already able to fight aggregates.
Maybe if we can improve them a little bit, we can significantly delay the onset of the severe disease.
Alzheimer's disease is classified according to Braak stages, and scientists found that it takes about 35 years to go from stage 3, where mild symptoms appear, to stage 6, the most advanced.
The aggregates grow exponentially, which explains why the disease takes so long to develop, and why people tend to get worse quickly, according to Georg Meisl.
The team wants to apply the same methods to study traumatic brain injury and frontotemporal dementia, in which tau protein also plays a role.
Hopefully this and other studies will help guide the development of future tau-targeted treatments, so they have a better chance of slowing the disease and helping people with dementia, Sara Imarisio of Alzheimer's Research UK said in a statement.
The paper, published in Science Advances, is the first to use human data to quantify the speed of molecular processes leading to this neurodegenerative disease, and could influence how treatments are designed.
It also overturns the theory that clusters form in a single location and trigger a chain reaction in other areas, a pattern seen in mice. Such spread can occur, but is not the primary driver, the researchers say.
Two things made this work possible, Georg Meisl, a chemist at the University of Cambridge and one of the lead authors of the paper, told AFP.
First, the study of very detailed data from PET scans (a type of medical imaging test, nldr) and various datasets collected, and the mathematical models that have been developed over the last 10 years.
The researchers used 400 brain samples taken after the death of people with Alzheimer's and 100 PET scans taken of people living with the disease to track tau protein aggregation.
Amyloid and another protein called beta-amyloid build up, causing brain cells to die and the brain to shrink.
This causes memory loss and an inability to perform daily tasks. The disease is a major public health problem, affecting more than 40 million people worldwide.
The researchers also found that it takes five years for the aggregates to double in number. This is an encouraging figure, according to Georg Meisl, because it shows that neurons are already able to fight aggregates.
Maybe if we can improve them a little bit, we can significantly delay the onset of the severe disease.
Alzheimer's disease is classified according to Braak stages, and scientists found that it takes about 35 years to go from stage 3, where mild symptoms appear, to stage 6, the most advanced.
The aggregates grow exponentially, which explains why the disease takes so long to develop, and why people tend to get worse quickly, according to Georg Meisl.
The team wants to apply the same methods to study traumatic brain injury and frontotemporal dementia, in which tau protein also plays a role.
Hopefully this and other studies will help guide the development of future tau-targeted treatments, so they have a better chance of slowing the disease and helping people with dementia, Sara Imarisio of Alzheimer's Research UK said in a statement.