Imagine going to a dance where Alzheimer’s disease and Type 2 diabetes are the star performers. In a recent study, scientists explored the genetic relationship between these two age-associated diseases. They searched for shared genes in order to uncover potential risk factors and pave the way for early diagnosis and prevention strategies. Interestingly, they discovered a tendency for North African populations to be underrepresented in genetic studies. By combing through a wealth of scientific literature, analyzing variant distributions, and investigating gene functions, they found 231 shared variants and 363 shared genes between Alzheimer’s disease and Type 2 diabetes. These genes are involved in important pathways related to protein binding, amyloid fibril deposition, microglia activation, and cholesterol metabolism. Furthermore, the study revealed several intriguing single nucleotide polymorphisms (SNPs) that may have pathogenic or regulatory effects in the brain. What’s more, they observed distinct patterns in North African populations compared to other worldwide populations. This research sheds light on the unique molecular architecture of North African populations when it comes to Alzheimer’s disease and Type 2 diabetes. To further unravel the fascinating connection between these two diseases, future investigation studies tailored to specific ethnicities are needed. Curious to learn more about this genetic tango? Be sure to explore the underlying research!

IntroductionAlzheimer’s disease (AD) and Type 2 diabetes (T2D) are both age-associated diseases. Identification of shared genes could help develop early diagnosis and preventive strategies. Although genetic background plays a crucial role in these diseases, we noticed an underrepresentation tendency of North African populations in omics studies.Materials and methodsFirst, we conducted a comprehensive review of genes and pathways shared between T2D and AD through PubMed. Then, the function of the identified genes and variants was investigated using annotation tools including PolyPhen2, RegulomeDB, and miRdSNP. Pathways enrichment analyses were performed with g:Profiler and EnrichmentMap. Next, we analyzed variant distributions in 16 worldwide populations using PLINK2, R, and STRUCTURE software. Finally, we performed an inter-ethnic comparison based on the minor allele frequency of T2D-AD common variants.ResultsA total of 59 eligible papers were included in our study. We found 231 variants and 363 genes shared between T2D and AD. Variant annotation revealed six single nucleotide polymorphisms (SNP) with a high pathogenic score, three SNPs with regulatory effects on the brain, and six SNPs with potential effects on miRNA-binding sites. The miRNAs affected were implicated in T2D, insulin signaling pathways, and AD. Moreover, replicated genes were significantly enriched in pathways related to plasma protein binding, positive regulation of amyloid fibril deposition, microglia activation, and cholesterol metabolism. Multidimensional screening performed based on the 363 shared genes showed that main North African populations are clustered together and are divergent from other worldwide populations. Interestingly, our results showed that 49 SNP associated with T2D and AD were present in North African populations. Among them, 11 variants located in DNM3, CFH, PPARG, ROHA, AGER, CLU, BDNF1, CST9, and PLCG1 genes display significant differences in risk allele frequencies between North African and other populations.ConclusionOur study highlighted the complexity and the unique molecular architecture of North African populations regarding T2D-AD shared genes. In conclusion, we emphasize the importance of T2D-AD shared genes and ethnicity-specific investigation studies for a better understanding of the link behind these diseases and to develop accurate diagnoses using personalized genetic biomarkers.

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