From: Elements4Health.
The results of a mouse study could lead to a new treatment for Alzheimer's disease that actually removes amyloid plaques from Alzheimer's brains.
Amyloid plaques are clumps of protein fragments that accumulate between the brain’s nerve cells and are considered a hallmark of Alzheimer's disease. There is currently no cure for Alzheimer’s disease.
This breakthrough discovery is based on the unexpected finding that when the brain's immune cells (microglia) are activated by the interleukin-6 protein (IL-6), they actually remove plaques instead of causing them or making them worse. The research was performed in a model of Alzheimer's disease established in mice.
The researchers made this unexpected discovery when they initially set out to prove that the activation of microgila trigger inflammation, making Alzheimer's disease worse. Their hypothesis was that microglia would attempt to remove the plaques, but would be unable to do so, and in the process cause excessive inflammation. To the surprise of the researchers, when microglia were activated by IL-6, they cleared the plaques from the brains.
To do this, the researchers over-expressed IL-6 in the brains of newborn mice that had yet to develop any amyloid plaques, as well in mice with pre-existing plaques. Using somatic brain transgenesis technology, scientists analyzed the effect of IL-6 on brain neuro-inflammation and plaque deposition. In both groups of mice, the presence of IL-6 lead to the clearance of amyloid plaques from the brain.
Researchers then set out to determine exactly how IL-6 worked to clear the plaques and discovered that the inflammation induced by IL-6 directed the microglia to express proteins that removed the plaques. This research suggests that manipulating the brain's own immune cells through inflammatory mediators could lead to new therapeutic approaches for the treatment of neurodegenerative diseases, particularly Alzheimer's disease.
References:
1. Pritam Das, et al. Massive gliosis induced by interleukin-6 suppresses A deposition in vivo: evidence against inflammation as a driving force for amyloid deposition. FASEB J. doi:10.1096/fj.09-141754.
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