Debris-gobbling immune cells can be enticed into the brain to eat away the amyloid plaques associated with Alzheimer鈥檚 disease, according to a study in mice.
The study suggests a promising new approach in the fight against Alzheimer鈥檚 鈥� and several drug candidates are already on pharmaceutical company shelves, waiting to be tried out.
at Yale University in New Haven, Connecticut, and his colleagues created a double transgenic mouse, dubbed Tg2576-CD11c-DNR. One gene predisposed it to develop amyloid plaques in its brain that mimic Alzheimer鈥檚 disease, while another blocked the activity of TGF-beta, a cytokine.
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The researchers had expected the double-transgenic mice to do even more poorly than their single-transgenic Alzheimer鈥檚 cagemates. But as the animals got to old age 鈥� about 18 months 鈥� the Tg2576-CD11c-DNR mice performed significantly better at traversing through various mazes. When the researchers examined their brains, they found up to 90% less amyloid.
For reasons that are not entirely clear, selectively blocking TGF-beta allowed macrophages, immune cells that ingest unwanted materials, to get across the blood brain barrier and into the brain. There, they feasted on amyloid plaques. 鈥淚t was like a vacuum cleaner,鈥� says Flavell.
Several drug candidates already exist that are known to block TGF-beta in a similar way. It鈥檚 too early to know if such a drug would be able to roll back the symptoms. 鈥淏ut even to reverse the decline would be an improvement,鈥� says Flavell.
Journal reference: , DOI: 10.1038/nm1781
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