Professor Donna Wilcock discusses an exciting finding from her research group that uses immunotherapy to prevent neurofibrillary tangles in mice.

We use amyloid beta immunotherapy as a potential therapeutic intervention in Alzheimer’s disease that would be disease-modifying, meaning that we are modifying one of the pathologies of Alzheimer’s disease. The way this works is just like when you get your measles shot when you are a child. You are given a piece of the measles virus, and your body responds to that to make antibodies, which make you immune so the next time your body sees measles, the antibodies will bind to it and your body removes it before you have any symptoms. So if you take that idea and you take it to Alzheimer’s disease, the approach that we have most recently used is to take the a-beta [amyloid beta] peptide that is a component of an amyloid plaque (the only component), and take this a-beta and stimulate the mouse in our case to make antibodies to the a-beta. So, now the mouse has anti-a-beta antibodies circulating, and by several different mechanisms that have been studied over the last ten years, we know that this antibody will bind to the a-beta and essentially target it for removal by the body. And so, the a-beta gets removed from the brain. What we have most recently shown is that, by doing this, we can now reduce the tau pathology, the neurofibrillary tangles, and we also prevent neuron loss. So this is really encouraging from a standpoint that we have been able to target one of the pathologies of Alzheimer’s disease and affect all of the pathologies of Alzheimer’s disease in a mouse model. And actually this is really the first mouse model that we’ve been able to test this in, because it’s the first mouse model that does have amyloid plaques, tau pathology, and neuron loss.

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