In a recent study published in PLOS ONE, researchers evaluated the association between Helicobacter pylori (H. pylori) infection and cognition amongst adult United Kingdom (UK) residents.

Study: Cognitive function in UK adults seropositive for Helicobacter pylori. Image Credit: SewCreamStudio/Shutterstock.com

Background

H. pylori, a gram-negative bacterial organism, infects the stomach and duodenum in humans. H. pylori infection mostly occurs during childhood, starting from asymptomatic to mild (e.g., abdominal pain and gastric distress) to severe (e.g., atrophic gastritis, peptic ulcers, and gastric malignancy) infection.

Along with their associations with gastric disease, Helicobacter pylori infections have been related to reduced cognitive functions in previous studies, including the US Centres for Disease Control and Prevention’s (US CDC) National Health and Examination Surveys (NHANES).

The association between infection with H. pylori and cognitive impairments could raise health concerns at the non-public and population levels, warranting further research.

Concerning the study

In the current cross-sectional study, researchers investigated whether Helicobacter pylori infections could alter adults’ cognitive performance.

The UK Biobank data, comprising data from 500,000 adults aged 40 to 70 years from population-level registries, were analyzed to find out the association between Helicobacter pylori serological positivity and intensity and cognitive performance in various neuropsychological tasks amongst adults.

Individuals who showed Helicobacter pylori serological positivity (i.e., either negative or positive for Helicobacter pylori) and serological intensity (i.e., antibody titers against Helicobacter pylori antigens) data and had undergone cognitive testing were included within the evaluation.

Individuals were considered H. pylori-seropositive in the event that they were positive for 2 of the six antibodies against vacuolating cytotoxin A (VacA), cytotoxin-associated antigen-A (CagA), chaperonin (GroEL), outer membrane proteins (OMP), UreA, and catalase antigens, determined using median fluorescence intensity (MFI).

Cognitive tasks included reasoning, numeric memory, pairs matching, matrix pattern completion, tower rearrangement, symbol-digit substitution, response time testing, and trails-numeric and alphanumeric assessments.

Multivariate linear regression modeling was performed with data adjustments for covariates resembling age, sex, race, ethnicity, income, level of education, body mass index (BMI), self-reported health, alcohol intake, and smoking habits.

Results and discussion

The sample population varied for the cognitive tasks, ranging between 379 and 6,785 individuals. In the most important sampled population, 30% were seropositive for Helicobacter pylori. The mean age of the study participants was 55 years; 55% were female, 95% were Whites, and 40% had attained college-level education.

Helicobacter pylori seropositivity and serointensity within the adjusted models were related to worsened reasoning and numeric memory with increased errors in pair matching but improved tower rearrangement performance. lnCagA was related to worsened logic and numeric memory, whereas InVacA, lnCatalase, and InUreA were related to worsened reasoning.

lnGroEL was related to worse reasoning but higher performance within the tower rearrangement task. The interactions between Helicobacter pylori and age, gender, and level of education were statistically significant.

Nonetheless, multivariate-level significant associations were observed just for the age covariate. Helicobacter pylori seropositivity was related to worse performance on incorrect Pairs matching and the Trails numeric tasks with advancing age.

The association between Helicobacter pylori seropositivity and cognition may very well be as a consequence of altered 5-methyltetrahydrofolate concentrations amongst H. pylori-infected individuals. H. pylori colonization within the gastrointestinal tract could alter the intestinal microbiota composition and bidirectional signaling mechanisms linked to the brain cells to change cognition.

H. pylori infections could also reduce vitamin B12 levels and absorption of folate, which have been related to elevated homocysteine concentrations, which, in turn, are related to cognitive alterations and dementia.

Probable explanations for the influence of Helicobacter pylori infection on the functions of the brain, resulting in lowered cognition, include T lymphocyte-mediated apoptosis, molecular mimicry of the human (host), inflammation resulting from the ingress of platelets, cytokines, eicosanoids, or acute phase protein molecules, and increased oxidative stress.

Other causes include Helicobacter pylori infection-induced amyloid deposition as a consequence of pathogenic organisms passing via an altered blood-brain barrier (BBB) communication.

The findings indicated that Helicobacter pylori infection may very well be a clinically significant risk factor for cognitive dysfunction and doubtless even dementia, given the widespread prevalence of Helicobacter pylori infections. Existing strategies for managing H. pylori infections make infection with H. pylori a modifiable risk factor for cognitive decay.

Conclusions

The study findings showed that H. pylori infections could also be related to worse cognitive function amongst adults aged between 40.0 and 70.0 years.

Worse performance on the reasoning task was probably the most consistently related to H. pylori. Catalase was the one H. pylori antigen not significantly related to cognitive function.

There have been fewer negative associations with performance on the numeric memory and pairs-matching incorrect tasks, and none on the symbol-digit substitution trails numeric and alphanumeric tasks.

The findings concord with previous studies and indicate that executive function could also be especially vulnerable to Helicobacter pylori infection.