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How toxic protein spreads in Alzheimer’s disease

Oskar Hansson (Photo: Kennet Ruona)
Oskar Hansson (Photo: Kennet Ruona)

Toxic versions of the protein tau are believed to cause death of neurons of the brain in Alzheimer’s disease. A new study published in Nature Communications shows that the spread of toxic tau in the human brain in elderly individuals may occur via connected neurons. The researchers could see that beta-amyloid facilitates the spread of toxic tau.

The present study is a collaboration between Lund University in Sweden and McGill University in Canada, and provides information on how toxic tau spreads in the human brain.

“Our research suggests that toxic tau may spread across different brain regions through direct neuronal connections, much like infectious diseases may spread to different cities through different transportation pathways. The spread is restricted during normal aging, but in Alzheimer’s disease the spread may be facilitated by beta-amyloid, and likely leads to widespread neuronal death and eventually dementia,” says lead author Jacob Vogel from McGill University.

“I think these findings have implications for therapies aiming at stopping the spread of tau and thereby halting the disease progression in Alzheimer’s,” says Oskar Hansson, professor of neurology at Lund University and co-lead investigator of the study.

There are two proteins that are known to be linked to Alzheimer's disease – beta-amyloid, which forms what is known as a plaque in the brain, and tau, which forms tangles within brain cells. Previous studies have linked the spread of toxic tau, in particular, to degeneration of the brain and symptoms such as memory impairment.

Intense research is ongoing to better understand how toxic tau spreads in the brain, in order to develop new therapies that can stop the spread and thereby stop the disease. Ongoing clinical trials are currently evaluating whether antibodies developed to bind to tau might stop the disease.

“Our findings have implications for understanding the disease, but more importantly for the development of therapies against Alzheimer’s, which are directed against either beta-amyloid or tau. Specifically, the results suggest that therapies that limit uptake of tau into the neurons or transportation or excretion of tau, could limit disease progression,” says Oskar Hansson.

The study was financed by the European Research, the Swedish Research Council, the Knut and Alice Wallenberg foundation, the Marianne and Marcus Wallenberg foundation, the Swedish Alzheimer Foundation, the Swedish Brain Foundation, the Swedish Medical Association, the Parkinson foundation of Sweden, the Skåne University Hospital, and the Swedish federal government under the ALF agreement.

Spread of pathological tau proteins through communicating neurons in human Alzheimer's disease

Oskar Hansson, professor of neurology, Clinical Memory Research Unit, Lund University, Sweden
+ 46 72 226 7745
oskar [dot] hansson [at] med [dot] lu [dot] se (oskar[dot]hansson[at]med[dot]lu[dot]se)

Jacob W. Vogel, PhD student, Montreal Neurological Institute, McGill University
jacob [dot] vogel [at] mail [dot] mcgill [dot] ca (jacob[dot]vogel[at]mail[dot]mcgill[dot]ca)




About the study:

The study involved 312 participants that represented a selection of individuals from two large multi-center studies: the Swedish BioFinder Study and ADNI, the Alzheimer’s Disease Neuroimaging Initiative. The researchers used positron emission tomograph (PET) to image toxic tau in living humans. Separately, they used MRI to map anatomical connections between brain regions. An epidemic spreading model (ESM) was fit to the data, simulating the spread of tau from a single epicenter through these anatomical connections over time. The tau patterns simulated by the model were highly correlated with the patterns observed in participants using PET.

“The MRI measures could only measure large-scale anatomical connections, not the individual axons that likely transport the toxic tau,” says Jacob Vogel.