- Scientists at The Picower Institute for Learning and Memory at MIT may have taken a significant step toward addressing inflammation, a particularly challenging aspect of Alzheimer’s disease.
- A new study reveals that a molecule called A11 can dampen inflammation and enhance cognitive function in human-like cells and Alzheimer’s mouse models.
- By targeting a gene transcription factor named PU.1 — known to become overactive in Alzheimer’s disease — A11 is able to inhibit the gene’s ability to promote inflammation in the brain’s microglial immune cells without interfering with its other crucial roles in the body.
This preliminary study, published in the Journal of Experimental Medicine, reveals that A11 effectively reduces inflammation in cells similar to human microglia and also in several Alzheimer’s mouse models, while notably enhancing cognitive function in the mice.
While there has been some advancement in treating Alzheimer’s disease through medications that lower amyloid-beta protein levels, other issues like inflammation remain unaddressed.
The new molecule, known as “A11,” aims to inhibit a genetic transcription factor named PU.1.
Previous studies have indicated that in the context of Alzheimer’s disease, PU.1 becomes excessively active in promoting inflammation through gene expression in the brain’s microglia immune cells.
According to the new findings, A11 curtails this problematic activity of PU.1 by enlisting other proteins to suppress the inflammatory genes that PU.1 is involved in activating.
The research group had previously conducted studies that identified PU.1 as a key factor in regulating excessive inflammation in microglia in Alzheimer’s mouse models.
This new research commenced with experiments designed to further confirm the therapeutic potential of targeting…
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