Could lack of an essential amino acid cause Alzheimer’s disease?

What causes Alzheimer’s disease? This question doesn’t have a simple answer but is one that researchers from Duke University, USA are one step closer to understanding. They have identified a mechanism behind neuronal dysfunction, which they believe could play a major role in Alzheimer’s disease symptoms.

Published in the Journal of Neuroscience, the researchers have found that lack of arginine, an amino acid essential for several bodily processes including cell division and healing, can also lead to immunosuppression in mice with Alzheimer’s disease. This essentially means that a lack of this amino acid could make your body less able to fight off foreign invaders, including the toxic proteins responsible for Alzheimer’s disease.

The research in brief

In this study, mice were genetically modified to develop the pathological signs of human Alzheimer’s disease including amyloid plaques, neurofibrillary tangles, hippocampal neuronal loss, and behavioural changes. The researchers were specifically interested in looking at the longitudinal changes in brain immunity in relation to neuronal loss.

The researchers found that neuronal death in the hippocampus (the brain’s memory centre) was largely due to the reduced levels of arginine. This caused immunosuppression in the mice which led to an increase in the number of CD11c microglia (these cells can enhance immunosuppression) and arginase, an enzyme that breaks down arginine and is highly expressed in regions of the brain involved in memory.

The scientists also went one step further. When they blocked arginase using an experimental drug, these mice developed fewer numbers of the CD11c microglia and amyloid beta plaques in the brains, and consequently they also performed better on memory tests.

The implications of this research?

The researchers now suggest that arginine levels could play a role in Alzheimer’s disease progression, particularly in relation to neuronal death, and could be considered a target for therapeutic development in the future.

However this study does not suggest that people should eat more foods which contain arginine or take dietary supplements, particularly as the results have only been seen in mice.

According to lead researcher on this study, Professor Carol Colton from the Duke University School of Medicine and a member of the Duke Institute for Brain Sciences, there is a dense mesh of cells and blood vessels called the blood-brain barrier which determine how much arginine will enter the brain. Eating more arginine may not help more of it get into the sites of the brain that need it. She also went on to say that if the scientists’ theory is correct, then the enzyme arginase, unless it’s blocked, would still break down the arginine.

More research is required to understand if a similar process happens in the brains of humans. Dementia News will keep you posted.


Journal of Neuroscience - http://www.jneurosci.org/content/35/15/5969.short
Duke University Media Release - https://today.duke.edu/2015/04/arginine



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