Tau Antibodies May Best Treat Alzheimer’s by Avoiding an Inflammatory Trigger

Tau Antibodies May Best Treat Alzheimer’s by Avoiding an Inflammatory Trigger
Researchers at Genentech discovered that antibodies against tau — a protein creating toxic tangles inside nerve cells of people with Alzheimer's disease — protect from tau toxicity only when antibodies don’t engage inflammation-triggering microglial cells to get rid of the protein. The findings, published in the journal Cell Reports under the title "Antibody-Mediated Targeting of Tau In Vivo Does Not Require Effector Function and Microglial Engagement," are likely to inform future attempts to develop anti-tau therapies for Alzheimer's, as well as a multitude of other conditions linked to an abnormal aggregation of tau. In addition to amyloid-beta, which accumulates outside neurons in patients with Alzheimer’s, researchers believe that the aggregation of tau protein inside nerve cells contributes to the toxic effects that kill cells in the brains of patients. Unlike amyloid plaque, the extent and distribution pattern of tau correlate with Alzheimer's symptoms and disease severity. Scientists know that tau aggregation can spread from cell to cell in a process involving the release of faulty tau from one cell that is then taken up by another, unaffected neuron. This process is believed to drive disease progression. Researchers have tried to develop antibodies that capture the protein when it is outside the cell, preventing it from spreading the tangles. An antibody response usually involves what researchers refer to as effector functions. On one side, the antibody — looking like the letter Y — binds a particular molecule. On the oth
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