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The聽publication of evidence that gum disease bacteria may cause Alzheimer鈥檚聽has prompted聽questions on social media about how seriously we should take the results. Here鈥檚 what you need to know about the landmark study.

Does the study show that the bacteria cause Alzheimer鈥檚 disease, or just that the two are linked in some way?

Any well-informed reader will know that correlation doesn鈥檛 mean causation, and not every link between two factors implies that one causes the other. But some do. Taken together, the new mouse experiments do suggest a causal link between the gum disease bacterium Porphyromonas gingivalis聽and Alzheimer鈥檚.

When the team gave these bacteria to mice, the animals developed dementia that looked like human Alzheimer鈥檚. The gingipain toxins produced by these bacteria activate certain parts of the immune system, and were found in this study to degrade tau protein. Both effects are known to produce Alzheimer鈥檚 symptoms.

And when the team gave these聽mice a drug that kills the bacteria, either directly or by blocking the gingipains they use to聽feed, there was a reduction both聽in bacteria and in symptoms. Together, these satisfy most of the conditions required to attribute a disease to a microorganism.

But that鈥檚 in mice 鈥� what about humans?

There are hints that the same聽may be true in humans. Nearly all of the 54聽Alzheimer鈥檚 brain samples studied by the team contained gingipains, and the more聽gingipains a person had, the more degraded tau protein they had聽鈥� a sign of worse Alzheimer鈥檚 symptoms while alive.

The team also found low levels of gingipains and damage in the brains of some people who didn鈥檛 have the condition, consistent with the fact that聽Alzheimer鈥檚 is the result of years of accumulating brain damage.

Isn鈥檛 this study too small to say anything?

While 54聽people isn鈥檛 a huge聽sample,聽it is large by the standards of much聽brain research, where tissue can be hard to get. Larger study sizes tend to come into play in later-stage clinical studies.

Can we trust a study from a pharmaceutical firm?

The study involved researchers from Cortexyme, a pharmaceutical firm in San Francisco that is developing treatments that interfere with P. gingivalis and its toxic gingipains. This led some online commenters to express doubts over whether the study can be 鈥渢rusted鈥�.

But the study was accepted by the peer-reviewed journal , and 14 of the 26 authors of the paper aren鈥檛 directly employed by Cortexyme.

Besides, many big pharma companies have pulled out of less profitable drug-development areas, including antibiotics and Alzheimer鈥檚, and Cortexyme is typical of the smaller firms that now do most early drug development. It is healthy to be sceptical, and聽much research is needed to confirm the study, but if we don鈥檛 trust commercial firms on principle, we will struggle to find ways to develop badly needed drugs.