Introduction: Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that profoundly affects both morbidity and mortality while placing a considerable economic strain on the healthcare system. Although the exact cause of AD remains
unknown, one hypothesis suggests that cytomegalovirus (CMV) may play a role in the disease’s development by driving
chronic neuroinflammation. The goal of this paper is to highlight the genetic factors associated with CMV that contribute to the progression of AD, with the goal of advancing future management and treatment strategies for this challenging
condition.
Methods: A search was performed using keywords like “Cytomegalovirus and Alzheimer’s Disease” and “Mechanisms of Alzheimer’s Disease and CMV Genetics.” This search identified 140 articles, which were then screened using DistillerRS. Articles specific to CMV genetic association to development and progression of AD were included, while others focused on other Herpes viruses were excluded.
Results: CMV may contribute to AD through a variety of different mechanisms. Seen in Figure 1., there are multiple genetic components of CMV that allow the virus to infect the host, suppress host immunity, and remain latent in host cells. In addition, CMV can penetrate the CNS by decreasing BBB permeability. This may be seen more in those who are infected more than once or may have a “superinfection” due to being in an immunocompromised state leading to neuronal damage.
Conclusion: The inflammatory response triggered by CMV infection in the brain could be a major factor in neurodegeneration associated with Alzheimer’s disease (AD). However, the diverse hypotheses suggest that CMV may play a multifaceted role in AD pathogenesis. Further research is essential to clarify the definitive relationship between CMV and AD, which is crucial for advancing diagnosis, management, and treatment strategies for the disease.
Methods: A search was performed using keywords like “Cytomegalovirus and Alzheimer’s Disease” and “Mechanisms of Alzheimer’s Disease and CMV Genetics.” This search identified 140 articles, which were then screened using DistillerRS. Articles specific to CMV genetic association to development and progression of AD were included, while others focused on other Herpes viruses were excluded.
Results: CMV may contribute to AD through a variety of different mechanisms. Seen in Figure 1., there are multiple genetic components of CMV that allow the virus to infect the host, suppress host immunity, and remain latent in host cells. In addition, CMV can penetrate the CNS by decreasing BBB permeability. This may be seen more in those who are infected more than once or may have a “superinfection” due to being in an immunocompromised state leading to neuronal damage.
Conclusion: The inflammatory response triggered by CMV infection in the brain could be a major factor in neurodegeneration associated with Alzheimer’s disease (AD). However, the diverse hypotheses suggest that CMV may play a multifaceted role in AD pathogenesis. Further research is essential to clarify the definitive relationship between CMV and AD, which is crucial for advancing diagnosis, management, and treatment strategies for the disease.