Encourage the immune system to be more effective in fighting diseases from the inside. Immunotherapy, from a strategy to fight tumors, is also moving towards neurodegenerative diseases. A new study also fits into this trend which uses an antibody to unblock immune cells in the central nervous system and thus push them to eliminate amyloid beta protein plaques – those aggregates believed to be the basis of brain degeneration and consequent cognitive decline in Alzheimer’s disease. The results, although preliminary, are promising: after treatment, behavioral anomalies decrease in the animal model.
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An “unblocking” antibody
As researchers at the Washington University School of Medicine in St. Louis explain on the pages of Science Translational Medicine, when aggregates of amyloid beta protein form, the brain’s immune cells, called microglia, rush to fulfill their purpose of preventing the expansion of the damage to the fabric. They should therefore engulf and eliminate the dangerous aggregates, but they do not do so, indeed, once they arrive on site, it is as if they were turned off. The reason, according to experts, is that in proximity to the amyloid plaque, microglial cells bind through a surface receptor (LILRB4) to the ApoE proteins present in the amyloid plaques. This bond acts as a sort of molecular switch and inactivates them.
On this basis, the researchers produced an antibody capable of preventing the binding between the ApoE protein and the LILRB4 receptor, which in animal models unblocked microglia, leading to a reduction in amyloid plaques and also a decrease in behavioral abnormalities.
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Alzheimer’s and beyond
Although preliminary, such results are very promising, according to the authors of the research, and it is also possible that the action of the antibody modifies the subsequent stages of the disease. The intention now is to test the new strategy on a different animal model, one in which amyloid proteins accumulate (as happens in humans) also at the level of the walls of the cerebral arteries, to verify whether their removal by of microglia can cause bleeding and swelling – a serious side effect already known from other (controversial) pharmacological strategies to combat Alzheimer’s.
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It’s not all. As Marco Colonna, head of the research, reports, by activating microglia in general, the type of antibody developed could potentially also eliminate other harmful proteins in the context of different neurodegenerative pathologies, such as Parkinson’s disease, amyotrophic lateral sclerosis (ALS) or the of Huntington.