Targeting the immune cells in the brain could slow down the onset of Altzheimer’s, a new study has shown.

The build-up of tau protein in the brain can be indicative many neurodegenerative disorders, including Alzheimer’s. Once the tau starts to clump together, tissue damage begins to become visible. However, until recently the link between protein build up and tissue damage was not known. A new study suggests that immune cells may be the missing piece of the puzzle.

Microalgia are the immune cells in the brain. Previous research has suggested that they are effective at preventing the toxic build-up of tau. However, new research has suggested that microalgia are a ‘double edge sword’ and their attempts to control the build-up of tau backfire to cause brain tissue damage.

Mice were genetically modified to produce a human form of tau that clumps together. The mice start forming tau clumps at 6 months and exhibit brain damage by 9. Certain mice were additionally genetically engineered with the human gene variant APOE4. Humans that have the gene variant have twelve times higher risk of developing Alzheimer’s, and previous research has found that APOE4 amplifies the damaging effects of tau on the brain.

The mice were fed a compound to deplete the microalgia cells in their brains, whilst others were fed a placebo. The mice that the high-risk variant APOE4 and their microalgia still present displayed shrunken and damaged brains by 9½ months. The mice with the high-risk variant and their microalgia depleted still had healthy brains and less tau tangles.

Furthermore, mice without APOE4 but non-depleted microalgia also displayed minimal brain damage. It was also found that the variant APOE4 was required to fully activate the microalgia. The researchers speculate that in response to rising numbers of tau clumps, the microalgia act to try and control them. However, in the process they cause major neuronal inflammation which leads to brain damage.

A drug that supresses the action of microalgia cells could therefore slow down the progression of Alzheimer’s.