ArticleBJPsych open2025
Association of CD33 genetic variants with neurocognitive profiles in chronic viral hepatitis.
Article in BJPsych open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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7 authors.
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Abstract
backgroundCD33 has been implicated in the pathogenesis of Alzheimer's disease primarily through its role in inhibiting the clearance of beta-amyloid (Aβ). However, genetic studies yield mixed results and it is unclear whether the impact of CD33 is specific to Alzheimer's disease or related to broader neurodegenerative processes. Interestingly, CD33 has also been shown to interact with the hepatitis B (HBV) and C viruses (HCV).
aimsThis study aims to investigate the effects of CD33 single-nucleotide polymorphisms (SNPs) on cognitive functions across diverse populations, including healthy controls, individuals with chronic HBV or HCV and those diagnosed with Parkinson's disease.
methodWe genotyped CD33 SNPs in 563 participants using the Affymetrix platform. Participants' cognitive functions were cross-sectionally assessed using a neuropsychological test battery spanning six domains.
resultsOur analysis revealed that CD33 SNP variations had no significant cognitive impact on healthy individuals or Parkinson's disease patients. However, chronic HBV and HCV patients exhibited significant cognitive differences, particularly in memory, related to CD33 SNP genotypes. Moderation analysis indicated a heightened influence of CD33 SNPs on cognitive functions in chronic HBV and HCV individuals. Our data also suggest that inflammation severity may modulate the cognitive effects in hepatitis patients with specific CD33 SNPs.
conclusionsThis study highlights the importance of CD33 SNPs in cognitive outcomes, emphasising their role in the context of chronic viral hepatitis. It contributes to understanding the cognitive profiles influenced by CD33 SNPs and posits CD33's potential contribution to neurodegenerative disease progression, potentially intensified by HBV/HCV-induced inflammation.
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