Alzheimer’s May Spread Through the Brain Like an Infection

A new research published in Brain shows that the damage causing protein in Alzheimer’s spreads through the brain like an infection. This protein, called tau, is considered responsible for killing the neurons. This is one of the causes of memory impairment.

This finding supports the transneuronal spread theory, i.e., spreading from neuron to neuron, that attempts to explain Alzheimer’s.  Such a spread has previously been seen in mice. It is being observed in humans for the first time. 

For the research, the team at Cambridge University, UK, imaged brains of 17 Alzheimer’s patients by combining two imaging techniques. This let them see where tau was building up and compare it with neuron connectivity in those regions. The results showed that tau was present in heavy concentrations in areas which had high connectivity between neurons. Thomas Cope, one of the authors of the study, said, “We come down quite strongly in favour of the idea that tau is starting in one place and moving across neurons and synapses to other places.”

Along with tau, another protein is considered responsible for Alzheimer’s, β-amyloid. While tau is considered responsible for killing neurons, β-amyloid forms plaques outside neurons.

Around 44 million people are estimated to suffer from some form of dementia worldwide, out of which 4 million are in India. Alzheimer’s is the most common form of dementia. The researchers believe that this discovery can help in finding ways to inhibit the spread of tau, and thus reduce the severity of Alzheimer’s. 

"In Alzheimer’s disease, the most common brain region for tau to first appear is the entorhinal cortex area, which is next to the hippocampus, the 'memory region’”, said Professor James Rowe, senior author on the study. "This is why the earliest symptoms in Alzheimer’s tend to be memory problems. But our study suggests that tau then spreads across the brain, infecting and destroying nerve cells as it goes, causing the patient’s symptoms to get progressively worse."

Others who read the study did note some shortcomings with it, such as the small sample size, and the fact that the researchers did not follow patients over time. If more observations had been made across time, tau’s spread could have been seen better, giving more conclusive evidence of the transneuronal spread theory. 

Cope said that the Cambridge team is now tracking more patients and will be making more observations across time.