In a recent study published in PLOS ONE, researchers evaluated the association between Helicobacter pylori (H. pylori) infection and cognition among 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 most commonly occurs during childhood, ranging from asymptomatic to mild (e.g., abdominal pain and gastric distress) to severe (e.g., atrophic gastritis, peptic ulcers, and gastric malignancy) infection.
In addition to their associations with gastric disease, Helicobacter pylori infections have been related to reduced cognitive functions in previous studies, including the United States 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 personal and population levels, warranting further research.
About the study
In the present 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 determine the association between Helicobacter pylori serological positivity and intensity and cognitive performance in various neuropsychological tasks among 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 in the analysis.
Individuals were considered H. pylori-seropositive if they were positive for two 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, reaction time testing, and trails-numeric and alphanumeric assessments.
Multivariate linear regression modeling was performed with data adjustments for covariates such as 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 largest 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 in 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 associated with worsened reasoning.
lnGroEL was related to worse reasoning but better performance in the tower rearrangement task. The interactions between Helicobacter pylori and age, gender, and level of education were statistically significant.
However, multivariate-level significant associations were observed only 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 could be due to altered 5-methyltetrahydrofolate concentrations among H. pylori-infected individuals. H. pylori colonization in the gastrointestinal tract could alter the intestinal microbiota composition and bidirectional signaling mechanisms linked to the brain cells to alter 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, leading to 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 due to pathogenic organisms passing via an altered blood-brain barrier (BBB) communication.
The findings indicated that Helicobacter pylori infection could be a clinically significant risk factor for cognitive dysfunction and probably 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 may be related to worse cognitive function among adults aged between 40.0 and 70.0 years.
Worse performance on the reasoning task was the most consistently associated with H. pylori. Catalase was the only H. pylori antigen not significantly related to cognitive function.
There were 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 may be especially vulnerable to Helicobacter pylori infection.
