New sequencing results from the post-mortem brains of Alzheimer's patients has revealed they may suffer from bacterial contamination
Leading on from prior work that determined the beta amyloid found in Alzheimer's brains may in part act as an antimicrobial response, new DNA sequencing results from a research team in the UK have hinted once again that bacterial infection within the brain may be driving the deadly inflammation seen in Alzheimer's brains.
"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. Neuroinflammation in the brain may be a reaction to the presence of bacteria"
A UK based team sequenced material from the brains of 8 patients known to have had Alzheimer's disease, alongside 6 brains of patients considered healthy prior to death. They used next-generation sequencing to scan for specific bacterial genes - which act as indicators of specific strains and populations. The results showed that the brains of Alzheimer's individuals had a differing set of bacterial species - with a much higher ratio of a type called Actinobacteria compared to Proteobacteria. Perhaps more importantly however Alzheimer's brains contained on average 7 times more bacteria, whereas healthy brains maintained a low level resembling that of normal blood sample results.
"Previous studies looking at bacteria in the Alzheimer's brain have primarily investigated specific bacterial species. 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"
What can extrapolate from this data? While these remain relatively small samples and only hint at a possible cause, it does lead to some important questions. Could the blood-brain barrier somehow be broken down in Alzheimer's patients, or is the ability to remove bacterial invaders somehow diminished? We will have to await further research to delve further into these questions. It certainly adds fuel to the theory of neuroinflammation and bacterial load being potentially the major driving factor of the disease however.
"We need quantitative studies on the bacterial presence in the brain. Larger numbers of brain samples are required, and future studies should also investigate if bacteria are involved in other neurodegenerative diseases involving neuroinflammation"
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