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Eurasian Journal of
Medicine and Oncology Helicobacter pylori infection and Alzheimer’s disease

If these SNPs do not adequately represent the genetic Availability of data
architecture of H. pylori infection, the validity of the causal
inferences could be compromised. Second, the potential Original data generated and analyzed during this study
for residual confounding remains a significant concern, are included in this published article or supplementary
as unmeasured factors may simultaneously influence material. Further inquiries can be directed to the
both AD and H. pylori infection, complicating result corresponding author.
interpretation. In addition, despite the strengths of MR in References
reducing confounding, it is important to note that potential
confounders, such as microbial communities and lifestyle 1. Malfertheiner P, Camargo MC, El-Omar E, et al. Helicobacter
factors, may still affect both AD and H. pylori infection. pylori infection. Nat Rev Dis Primers. 2023;9(1):19.
These factors were not included in our analysis, which doi: 10.1038/s41572-023-00431-8
could influence the explanatory power. Moreover, the fact 2. Usui Y, Taniyama Y, Endo M, et al. Helicobacter pylori,
that the population in this study is exclusively European homologous-recombination genes, and gastric cancer.
limits the generalizability of the findings to other racial N Engl J Med. 2023;388(13):1181-1190.
and ethnic groups. It remains unclear whether the results
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5. Conclusion 4. Gorlé N, Bauwens E, Haesebrouck F, Smet A,
Vandenbroucke RE. Helicobacter and the potential role in
This investigation indicates a strong correlation among neurological disorders: There is more than Helicobacter
AD and anti-H. pylori UREA antibodies, suggesting a pylori. Front Immunol. 2020;11:584165.
potential role of H. pylori infection in the etiology of AD. doi: 10.3389/fimmu.2020.584165
These findings suggest H. pylori as a modifiable risk factor,
emphasizing the necessity for additional investigations to 5. Ju Z, Shen L, Zhou M, et al. Helicobacter pylori and Alzheimer’s
clarify causal mechanisms and address existing limitations. disease-related metabolic dysfunction: Activation of TLR4/
Myd88 inflammation pathway from p53 perspective and a
Acknowledgments case study of low-dose radiation intervention. ACS Chem
Neurosci. 2022;13(7):1065-1081.
None.
doi: 10.1021/acschemneuro.2c00082
Funding 6. Scheltens P, De Strooper B, Kivipelto M, et al. Alzheimer’s
None. disease. Lancet. 2021;397(10284):1577-1590.
doi: 10.1016/s0140-6736(20)32205-4
Conflict of interest
7. Tatulian SA. Challenges and hopes for Alzheimer’s disease.
The authors declare that they have no conflict of interest. Drug Discov Today. 2022;27(4):1027-1043.
Author contributions doi: 10.1016/j.drudis.2022.01.016

Conceptualization: Ke Yi 8. Trejo-Lopez JA, Yachnis AT, Prokop S. Neuropathology of
Alzheimer’s disease. Neurotherapeutics. 2022;19(1):173-185.
Formal analysis: Yuan Xin Hou, Ke Yi
Methodology: Yuan Xin Hou, Ke Yi doi: 10.1007/s13311-021-01146-y
Writing – original draft: Yuan Xin Hou, Ao Wang 9. Rostagno AA. Pathogenesis of Alzheimer’s disease. Int J Mol
Writing – review & editing: Yuan Xin Hou, Ao Wang Sci. 2022;24(1):107.
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Not applicable. 10. Vaz M, Silvestre S. Alzheimer’s disease: Recent treatment
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Not applicable. 11. Cuomo P, Papaianni M, Sansone C, et al. An in vitro model to

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