Blocking a key protein may help to prevent Alzheimer’s disease to take hold and spread, according to a study that used the latest grain imaging technology.
Scientists at the University of Cambridge used a combination of imaging techniques to examine how patterns of tau – the abnormal protein that destroys the nerve cells – relate to the wiring of the brain in 17 patients with Alzheimer’s disease, compared to controls.
Thanks to developments in positron emission tomography (PET) scanning, the team was able to test the different hypotheses as to how tau spreads.
One suggestion is transneuronal spread – that it begins in one place and then spreads to other regions, setting off a chain reaction. A second hypothesis – the metabolic vulnerability’ hypothesis – suggests that tau is made locally in nerve cells and that some regions have higher metabolic demands and are more vulnerable to the protein.
A third hypothesis, ‘trophic support’, claims that some brain regions are more vulnerable than others, thanks to a lack of nutrition to the region or with gene expression patterns.
First author Dr Thomas Cope from the university’s Department of Clinical Neurosciences and colleagues looked at the functional connections within the brains of the Alzheimer’s patients and compared this against levels of tau.
Writing in Brain, they say their findings supported the idea of transneuronal spread.
"If the idea of transneuronal spread is correct, then the areas of the brain that are most highly connected should have the largest build-up of tau and will pass it on to their connections,” said Dr Cope.
“It’s the same as we might see in a flu epidemic, for example – the people with the largest networks are most likely to catch flu and then to pass it on to others. And this is exactly what we saw."
Senior author Professor James Rowe, added: "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’.
“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."
The authors said that confirming the transneuronal spread hypothesis is important because it means that suggests that work can continue on slowing down or halting the progression of Alzheimer’s disease by developing drugs to stop tau from moving along neurons.
Cope, TE et al. Tau Burden and the Functional Connectome in Alzheimer’s Disease and Progressive Supranuclear Palsy. Brain 5 Jan 2018; doi: 10.1093/brain/awx347
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