Can Brain Bacteria Contribute to Alzheimer’s? These Researchers Think So

Joana Fernandes, PhD avatar

by Joana Fernandes, PhD |

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Patients with Alzheimer’s disease may have more bacteria — and different types — in their brains, compared to the general population, according to results of a new study. These findings support that bacterial infection and inflammation may contribute to the development of this devastating disease.

The study is titled “16S rRNA Next Generation Sequencing Analysis Shows Bacteria in Alzheimer’s Post-Mortem Brain” and was published in the journal Frontiers in Aging Neuroscience.

Neuroinflammation is one the mechanisms known to be active in Alzheimer’s disease. This reflects the body’s response to eliminate toxic factors, but too much of it ends up killing neurons.

“Alzheimer’s brains usually contain evidence of neuroinflammation, and researchers increasingly think that this could be a possible driver of the disease, by causing neurons in the brain to degenerate,” David Emery, the study’s first author, said in a press release.

According to Emery, this inflammatory response may be caused by the presence of bacteria in the brain. In a normal brain, this would not happen because of the meninges, the three tissue layers that protect the brain by regulating which molecules go in and out. However, in the Alzheimer’s brain, certain blood vessels lose their integrity, allowing bacteria to enter and settle in.

“Previous studies looking at bacteria in the Alzheimer’s brain have primarily investigated specific bacterial species,” said Shelley Allen, another study author. “We wanted to use an unbiased method to obtain the fullest overview possible of the entire bacterial population in the Alzheimer’s brain, and compare these results with those from a healthy aged brain.”

Using DNA sequencing techniques and post-mortem brain samples from eight patients with Alzheimer’s disease and six healthy subjects, researchers were able to detect specific bacterial genes at the same time, thus having an overview of different bacterial populations.

Results indicated that Alzheimer’s brains contained 10 times the amount of a specific bacteria than the healthy brains.

“Comparing the bacterial populations showed at least a tenfold higher ratio overall of Actinobacteria (mostly P. acnes) to Proteobacteria in the Alzheimer’s brain compared with the healthy brain,” Emery said.

Also, Alzheimer’s brains had more bacteria than the control samples.

“Unexpectedly, Alzheimer’s brains gave on average an apparent 7-fold increase in bacterial sequences above that seen in the healthy brain,” Allen said. “The healthy brains yielded only low levels of bacterial sequences, consistent with either a background signal or normal levels present in the bloodstream in brain tissue.”

Overall, these findings suggest an increase in bacterial populations in the Alzheimer’s brain tissue compared with normal brain tissue, but more studies are necessary to clarify the involvement of bacteria in the general pathology.

“We need quantitative studies on the bacterial presence in the brain,” said Allen. “Larger numbers of brain samples are required, and future studies should also investigate if bacteria are involved in other neurodegenerative diseases involving neuroinflammation.”