Summary: A new study reveals a potential link between Helicobacter pylori infection and an increased risk of Alzheimer’s disease.
Analyzing three decades of patient data, the researchers found that people over 50 with symptomatic H. pylori infection face an 11% higher risk of developing Alzheimer’s, which escalates to 24% a decade post-infection.
The study highlights H. pylori as a possible modifiable risk factor for Alzheimer’s, suggesting new avenues for prevention and treatment strategies.
- Symptomatic Helicobacter pylori infections after age 50 are associated with an 11% increased risk of Alzheimer’s, peaking at 24% after a decade.
- The study, covering over four million people, suggests H. pylori could be a modifiable risk factor for Alzheimer’s disease.
- H. pylori is known to potentially reach the brain, causing inflammation and neuron damage, and impairing absorption of Vitamin B12 and iron.
Infection with the stomach bacterium Helicobacter pylori could increase the risk of developing Alzheimer’s disease: In people over the age of 50, the risk following a symptomatic infection can be an average of 11 percent higher, and even more about ten years after the infection, at 24 percent greater risk.
These are the findings of a study by Charité – Universitätsmedizin Berlin and McGill University (Canada), now published in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. The researchers analyzed three decades’ worth of patient data.
As today’s populations age, dementia is set to become more common, tripling in prevalence in the next 40 years. With no cure in sight so far, researchers are trying to pinpoint the risk factors involved in dementia, in hopes of specifically targeting those factors.
Helicobacter pylori enters the central nervous system
Researchers have long suspected Helicobacter pylori, a common gut microbe, of being a potential risk factor. Nearly one-third of all people in Germany are infected with this type of bacteria. An infection can be asymptomatic, but the bacteria can also cause inflammation of the stomach lining or even stomach cancer.
Numerous lab studies have also found a link between H. pylori infection and the central nervous system.
“We know that the bacterium can reach the brain via various routes, potentially causing inflammation, damage, and the destruction of neurons there,” explains Prof. Antonios Douros, a pharmacoepidemiologist at Charité and the first author of the study.
When the stomach has been damaged by these microbes, it is also no longer able to absorb Vitamin B12 or iron effectively, which also increases the risk of dementia.
However, many of the studies performed to date on the association between H. pylori infection and Alzheimer’s disease suffered from methodological limitations – for example because the number of people studied was simply too low.
One outcome of this was that before now, it was also not possible to say just how strong a link there is between this type of bacterial infection and Alzheimer’s disease.
Representative study of over four million people
Douros, Prof. Paul Brassard of McGill University in Montreal, and their colleagues have now compensated for those limitations. Not only did their study have a very large sample size, at over four million people, but it also considered the time interval between infection and a possible increase in the risk of Alzheimer’s disease.
The researchers used data gleaned from electronic patient records in the UK to quantify the link between H. pylori and Alzheimer’s disease over the course of a person’s lifetime.
“Our study shows that symptomatic infections with H. pylori after the age of 50 can be associated with an eleven percent increase in the risk of Alzheimer’s disease. The risk increase peaks at 24 percent about a decade after the initial infection,” Douros says, summarizing the team’s findings.
But that doesn’t mean everyone who has experienced a symptomatic infection will necessarily go on to develop Alzheimer’s disease. The calculations show an increase in the relative risk compared to people who did not experience a symptomatic H. pylori infection after the age of 50.
Are H. pylori infections a modifiable risk factor?
“To us, this finding reinforces the assumption that an H. pylori infection could be a modifiable risk factor for Alzheimer’s disease,” Douros concludes.
However, the researchers caution that whether efforts to eradicate this gut microbe might actually affect the development of Alzheimer’s disease, and if so to what extent, would need to be tested in large-scale randomized studies first.
About this bacteria and Alzheimer’s disease research news
Author: Manuela Zingl
Contact: Manuela Zingl – Charite
Image: The image is credited to Neuroscience News
Original Research: Open access.
“Clinically apparent Helicobacter pylori infection and the risk of incident Alzheimer’s disease: a population-based nested case-control study” by Antonios Douros et al. Alzheimer’s & Dementia
Clinically apparent Helicobacter pylori infection and the risk of incident Alzheimer’s disease: a population-based nested case-control study
Our population-based study assessed whether clinically apparent Helicobacter pylori infection (CAHPI) is associated with the risk of Alzheimer’s disease (AD).
We assembled a population-based cohort of all dementia-free subjects in the United Kingdom’s Clinical Practice Research Datalink (UK CPRD), aged ≥50 years (1988–2017). Using a nested case-control approach, we matched each newly developed case of AD with 40 controls. Conditional logistic regression estimated odds ratios (ORs) with 95% confidence intervals (CIs) of AD associated with CAHPI compared with no CAHPI during ≥2 years before the index date. We also used salmonellosis as a negative control exposure.
Among 4,262,092 dementia-free subjects, 40,455 developed AD after a mean 11 years of follow-up. CAHPI was associated with an increased risk of AD (OR, 1.11; 95% CI, 1.01–1.21) compared with no CAHPI. Salmonellosis was not associated with the risk of AD (OR, 1.03; 95% CI, 0.82–1.29).
CAHPI was associated with a moderately increased risk of AD.