A new study out of Duke University, published in the Journal of Neuroscience, may provide new insight into one of the possible causes of Alzheimer’s disease (AD). This could lead to new, more effective treatments, and renews hope that the disease may one day be curable.
This study was done on mice that have Alzheimer’s and were genetically altered to make their immune systems more like that of a human.
The study suggests that, while there was already some evidence that the immune system played some kind of role in the development of Alzheimer’s, that role may have been different than what scientists have thought until now. It was once thought that the immune system was essentially going into overdrive and attacking brain tissue, but this study suggests that it is possible that, in fact, the suppression of the immune system may be in part to blame.
One of the most visible effects of Alzheimer’s disease is the development of sticky proteins on the brain tissue, known as brain plaques. For years, this was considered not only to be an indicator of Alzheimer’s, but one of the possible causes. It has been the focus of the majority of research for the last 10-15 years. This study suggests, however, that once those plaques become visible, irreparable damage may have already been done to the cells and neurological pathways, and that the plaque itself may not be causing symptoms.
It appears from this new study that some of the immune cells that usually protect the brain are “going rogue” and beginning to consume an amino acid called arginine, which plays an important part in basic biological functions like cell division, healing, and immune responses.
When the mice were then treated with a cancer drug called difluoromethylornithine (DFMO), it stopped those cells from consuming the arginine. The damage to the brain cells and the buildup of sticky plaques on the brain was prevented, and memory loss did not occur, and Alzheimer’s never developed in those mice.
Now, obviously, just because it worked on mice does not necessarily mean that it will work the same way on humans. But this study could change the way scientists think about Alzheimer’s disease and lead to new breakthroughs in the study of the disease.
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