Apolipoprotein ɛ4 Allele and Dental Occlusion Deficiency as Risk Factors for Alzheimer’s Disease

  • Popovac A
  • Mladenović I
  • Krunić J
  • et al.
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Compromised dentition has been suggested to pose a significant risk factor for dementia. It was mainly investigated through insufficient tooth number, disregarding contact between opposing teeth (dental occlusion). The epsilon 4 allele of apolipoprotein (APOE4) is the primary genetic marker for the late onset of Alzheimer's disease (AD). However, APOE4 and dental occlusion have not yet been investigated as possible associated risk factors for AD. The study was aimed to examine the impact of dental status and different APOE gene variants on AD occurrence. Secondly, sociodemographic variables were investigated as factors potentially associated with AD. The case-control study included two groups: 116 patients with AD (according to the NINDS-ADRDA criteria) and 63 controls (Mini-Mental State Examination scores >= 24). The analysis of APOE gene polymorphism was conducted through PCR reaction. Dental examination included recording of number of teeth, presence of fixed or removable dentures, and number of functional tooth units (FTU). Regression analysis was used to investigate the joint effect of the clinical and genetic variables on AD. Results showed that patients with AD were more often carriers of epsilon 3/epsilon 4 genotype and epsilon 4 allele, had lower number of teeth and FTU, and were less likely to be married, live in home, and had less chronic diseases, compared to the controls. Regression analysis showed that presence of APOE4 allele and the number of total FTU remained associated with AD, even when adjusted for age, sex, and level of education. In conclusion, deficient dental occlusion and presence of APOE4 may independently increase risk for AD.




Popovac, A., Mladenović, I., Krunić, J., Trifković, B., Todorović, A., Milašin, J., … Stančić, I. (2020). Apolipoprotein ɛ4 Allele and Dental Occlusion Deficiency as Risk Factors for Alzheimer’s Disease. Journal of Alzheimer’s Disease, 74(3), 797–802. https://doi.org/10.3233/jad-191283

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