ABI3 gene may be the key to new Alzheimer’s disease therapies
The study found that deleting the ABI3 gene in mice increased plaques and inflammation in the brain, suggesting avenues for new treatments.
Researchers at the Indiana University School of Medicine, US, have discovered that deleting the gene called ABI3 significantly increases amyloid-beta plaque accumulation in the brain and decreases the amount of microglia around the plaques. According to the team, this discovery could lead to the development of novel Alzheimer’s disease treatments in the future.
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The team based their research on a human genetics study of more than 85,000 people — fewer than half of whom were Alzheimer’s patients — that identified the mutation in the ABI3 gene. The researchers concluded that this mutation increased the risk of late-onset Alzheimer’s. “However, there was no investigation into the function of ABI3 gene in the brain or about how this gene affects microglia function,” added Dr Hande Karahan who co-led the research with Dr Jungsu Kim.
In this study, published in Science Advances, the team deleted the ABI3 gene from an Alzheimer’s disease mouse model and tested the functions of the gene in microglia in cell cultures. In the mouse model, they saw increased levels of plaques and inflammation in the brain and signs of synaptic dysfunction. Additionally, Karahan explained that the deletion of the gene impaired the movement of microglia so the immune cells cannot move closer to plaques to try to clear up the proteins.
“Our study provides the first in vivo functional evidence that the loss of ABI3 function may increase the risk of developing Alzheimer’s disease by affecting amyloid beta accumulation and neuroinflammation,” Karahan concluded. “This study can provide further insight into understanding the key functions of microglia contributing to the disease and help identify new therapeutic targets.”
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