For the first time, scientists have produced evidence in living humans that the protein tau, which mars the brain in Alzheimer’s disease, spreads from neuron to neuron.
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Researchers at the University of Cambridge in the United Kingdom combined two brain imaging techniques, functional magnetic resonance imaging and positron emission tomography (PET) scanning, in 17 Alzheimer’s patients to map both the buildup of tau and their brains’ functional connectivity—that is, how spatially separated brain regions communicate with each other. Strikingly, they found the largest concentrations of the damaging tau protein in brain regions heavily wired to others, suggesting that tau may spread in a way analogous to influenza during an epidemic.
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The research team says this pattern, described [January 5] in Brain, supports something known as the “transneuronal spread” hypothesis for Alzheimer’s disease, which had previously been demonstrated in mice but not people. “We come down quite strongly in favor of the idea that tau is starting in one place and moving across neurons and synapses to other places,” says clinical neurologist Thomas Cope.
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The spread of tau could have implications for clinical care, he adds, if drugs can be developed that attack tau in synapses, outside of cells, locking it up inside affected cells early, before it can spread.
Read full, original post: Alzheimer’s protein may spread like an infection, human brain scans suggest
