A paper published in The Journal of Neuroscience has analysed the profiles of chemicals involved in immune signalling in mice which are used as a model of Alzheimer’s disease. The researchers report that the disease is associated with an immunosuppressive pattern, in contrast to previous views which see the disease driven by immunity and inflammation. The study also reports low levels of a particular component of proteins in the brains of affected mice, and drugs which countered this also reduced measures of the disease and presence of immunosuppressive cells.
Dr Tara Spires-Jones, Reader, Centre for Cognitive and Neural Systems, University of Edinburgh, said:
“This nice study by Kan et al. adds to our knowledge of the complex role of the immune system in the development of Alzheimer’s-like brain changes in a mouse model. The results from this study, while very interesting, need to be confirmed in other models before moving into human studies to investigate whether these immune-mediated changes in arginine levels in mice are also important in people with Alzheimer’s.”
Dr James Pickett, Head of Research at Alzheimer’s Society said:
“This study in animals joins some of the dots in our incomplete understanding of the processes that cause Alzheimer’s disease, in particular around the role played by the immune system.
“Using a new animal model of Alzheimer’s, the researchers have found that depletion of a nutrient called arginine occurs in the damaged brain areas. Blocking the use of arginine reduced some of the disease hallmarks and improved memory performance, offering hope that these findings could lead to new treatments for dementia.
“Importantly, these new findings reflect earlier observations that arginine is reduced in the brains of people with Alzheimer’s disease. The next step would be to show that targeting arginine metabolism in the brain can reduce the death of brain cells, as this was not shown in the current study.”
Dr Laura Phipps, Science Communications Manager, Alzheimer’s Research UK, said:
“This interesting study sheds more light on the mechanisms of immune system involvement in Alzheimer’s, adding important insight to a growing body of research in this area. The research is in mice, so it will be important to build on the findings with further studies in humans. Clinical trials are essential before any potential new treatment can be given to people, but these early findings could open new doors for future treatment development for Alzheimer’s.
“The study suggests that low levels of arginine in the brain could contribute to the death of nerve cells in Alzheimer’s, but there is much more we still need to understand about how and why nerve cells die in the disease. Arginine is produced by the body, as well as being consumed through diet, and while it was implicated in this research study, the findings do not suggest that supplementation of the amino acid could mirror the benefits seen in these mice. Current research suggests that the best way to maintain a healthy brain throughout life is to ensure a balanced diet, not smoke, keep mentally and physically active and exercise regularly, and to keep blood pressure and cholesterol in check.”
‘Arginine Deprivation and Immune Suppression in a Mouse Model of Alzheimer’s Disease’ by Kan et al. published in The Journal of Neuroscience on Tuesday 14th April.
Dr Tara Spires-Jones: I am paid by the University of Edinburgh and am funded by Alzheimer’s Research UK, the University of Edinburgh and an anonymous foundation. I am on the Alzheimer’s Research UK Grants Advisory Board, am a member of the Journal of Neuroscience Editorial Board, and a member of SFN, FENS and BNA. I collaborate with Cognition Therapeutics, a pharmaceutical company in the US (not paid except occasional advisory board meeting compensation).
No other interests declared.