Infections, genetics, and Alzheimer's disease: Exploring the pathogenic factors for innovative therapies

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative condition that creates a significant global health challenge and profoundly affects patients and their families. Recent research has highlighted the critical role of microorganisms, particularly viral infections, in the pathogenesis of AD. The involvement of viral infections in AD pathogenesis is predominantly attributed to their ability to induce neuroinflammation and amyloid beta (Aβ) deposition in the brain. The extant research exploring the relationship between viruses and AD has focused largely on Herpesviridae family. Traces of Herpesviruses, such as Herpes Simplex Virus-1 and Epstein Barr Virus, have been found in the brains of patients with AD. These viruses are thought to contribute to the disease progression by triggering chronic inflammatory responses in the brain. They can remain dormant in the brain, and become reactivated due to stress, a secondary viral infection, or immune-senescence in older adults. This review focuses on the association between Herpesviridae and bacterial infections with AD. We explore the genetic factors that might regulate viral illness and discuss clinical trials investigating antiviral and anti-inflammatory agents as possible therapeutic strategies to mitigate cognitive decline in patients with AD. In summary, understanding the interplay between infections, genetic factors, and AD pathogenesis may pave the way for novel therapeutic approaches, facilitating better management and possibly even prevent this debilitating disease.

Keywords: Alzheimer's disease; Amyloid beta deposition; Anti-inflammatory agents; Antiviral agents; Herpesviridae family; Neurodegenerative disorder; Neuroinflammation; Pathogenesis; Viral infection.