It’s been just over a month since Amgen and Novartis ended two studies of an experimental Alzheimer’s treatment early, the latest in a long string of failures in Alzheimer’s drug development.
There is still no effective treatment for the disease. But as the population ages, the already significant need for an Alzheimer’s treatment is only growing more urgent, said Dr. David Reese, executive vice president of research and development at Amgen.
“The Alzheimer’s epidemic is a slow-moving tsunami that is going to swamp society over a period of two or three decades. We have to get ahead of that,” said Reese.
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A new study (21 Aug 2019) finds that “removing brain immune cells known as microglia from rodent models of Alzheimer’s disease, beta-amyloid plaques – the hallmark pathology of AD – never formed.”
Link between brain immune cells and Alzheimer’s disease development identified
https://news.uci.edu/2019/08/21/link-between-brain-immune-cells-and-alzheimers-disease-development-identified/
Meanwhile, in another recent study making waves, “In vitro data revealed that gal3 was required to fully activate microglia in response to fibrillar Aβ”
https://link.springer.com/article/10.1007%2Fs00401-019-02013-z
This raises the question whether beta-amyloid plaques accumulate in a self-reinforcing feedback cycle that is dependent upon Galectin-3 activation of microglia.
Galectin-3 inhibition should be investigated, for example GR-MD-02 (belapectin) which is currently entering Phase 3 for advanced NASH fibrosis. There appears to be a common mechanism between inflammation and fibrosis of other organs and of AD.