-Antibodies that block the deposition of amyloid (Aβ) protein were once thought to have played a key role in the treatment of Alzheimer's disease, but they did not effectively remove the deposited protein that previously existed in the patient's body. Shows that a modified antibody can be used to remove the already existing Aβ protein in the Alzheimer's disease mouse model. Related research results were published in the international journal Neuron.
A sign of Alzheimer's disease is the accumulation of amyloid plaques in nerve cells. One potential immunotherapy for Alzheimer's disease is the use of antibodies to target therapy to remove insoluble Aβ protein. Up to now, many researchers have used antibodies to bind soluble or insoluble Aβ protein. These antibodies are essential for reducing the deposition of Aβ protein in mouse models, but this is limited to giving mouse models a preventive measure. To prevent disease, this treatment does not seem to be very effective for mice that already have an amyloid deposit.
Researcher DeMattos hypothesized that these antibodies would not be able to remove protein plaques, because when they enter the brain, their binding to Aβ protein is saturated. To test this hypothesis, the researchers developed another genetically engineered antibody to selectively target protein plaques.
The researchers found that plaque-specific antibodies that cross the blood-brain barrier can bind to the deposited beta amyloid protein and promote the rapid removal of pre-existing plaque. The results show that it can only bind to insoluble amyloid beta The antibody is very important for the removal of plaque, and does not have any side effects.
New research findings can help researchers develop new treatments for Alzheimer's disease, which also explains why bapineuzumab, an Alzheimer's disease drug, did not have a placebo in two clinical trials and so on. Bapineuzumab can be combined with soluble or insoluble beta amyloid protein.
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