Imagine the human body as a complex puzzle. Well, scientists have discovered a key piece of that puzzle called the CD2AP gene and its connection to Alzheimer’s disease (AD). In previous studies, researchers found that a specific genetic variation, known as rs9349407 polymorphism, was linked to AD in people of European descent. Now, a team of Chinese scientists wanted to investigate if this association holds true for the Chinese population. They compiled data from 11 independent studies and conducted a meta-analysis, which revealed an interesting finding. It turns out that the CD2AP rs9349407 polymorphism does increase susceptibility to AD in Chinese populations, similar to what has been observed in Caucasian populations. The study also examined different ways this genetic variation affects AD susceptibility, such as under the additive model or the dominant model. This research provides valuable insights into the underlying genetic factors contributing to AD in the Chinese population. Nonetheless, more research with larger sample sizes is needed to confirm these findings and further unravel the intricate puzzle of Alzheimer’s disease.
BackgroundSince 2011, three large-scale genome-wide association studies (GWAS) have confirmed that the CD2AP rs9349407 polymorphism is significantly connected with Alzheimer’s disease (AD) in individuals of European descent. Subsequently, this association has been replicated in European populations, but is unclear whether it can be replicated in Chinese. Recently, the correlation between rs9349407 and AD in the Chinese population has become a research hotspot.ObjectiveTo explore the association between rs9349407 polymorphism and AD in the Chinese population.Materials and methodsFirstly, based on the exclusion and inclusion criteria, we selected 11 independent studies from 8 articles exploring the correlation between rs9349407 variation and AD in Chinese. Secondly, we conducted a meta-analysis based on fixed and random effect models and conducted a heterogeneity test. Thirdly, we used the additive model, dominant model, and recessive model for subgroup analysis.ResultsWe demonstrated that the CD2AP rs9349407 polymorphism increases AD susceptibility in Chinese populations (OR = 1.33, 95% CI = 1.08–1.64, P = 7.45E-03), which is consistent with the effect observed in Caucasian populations. Additionally, subgroup analysis showed that rs9349407 under the additive model (GG + CC vs. GC, OR = 0.76, 95% CI = 0.61–0.97, P = 2.04E-02) and dominant model (GG + GC vs. CC, OR = 0.49, 95% CI = 0.32–0.74, P = 8.51E-04) were also significantly correlated with AD susceptibility, but not under the recessive model (GG vs. GC + CC, OR = 0.77, 95% CI = 0.58–1.03, P = 7.44E-02).ConclusionThese existing data suggest that rs9349307 is significantly correlated with the susceptibility to AD in the Chinese population, but future studies with large samples are needed to confirm our findings.
Dr. David Lowemann, M.Sc, Ph.D., is a co-founder of the Institute for the Future of Human Potential, where he leads the charge in pioneering Self-Enhancement Science for the Success of Society. With a keen interest in exploring the untapped potential of the human mind, Dr. Lowemann has dedicated his career to pushing the boundaries of human capabilities and understanding.
Armed with a Master of Science degree and a Ph.D. in his field, Dr. Lowemann has consistently been at the forefront of research and innovation, delving into ways to optimize human performance, cognition, and overall well-being. His work at the Institute revolves around a profound commitment to harnessing cutting-edge science and technology to help individuals lead more fulfilling and intelligent lives.
Dr. Lowemann’s influence extends to the educational platform BetterSmarter.me, where he shares his insights, findings, and personal development strategies with a broader audience. His ongoing mission is shaping the way we perceive and leverage the vast capacities of the human mind, offering invaluable contributions to society’s overall success and collective well-being.