The emerging mechanism behind viral infections and extracellular vesicles hypotheses leading to neuroinflammation and Alzheimer's disease pathology. Issue 1 (31st January 2023)

• Record Type: Journal Article
• Authors: Anwar, Mai M.
• Is Part Of: Ibrain. Volume 9:Issue 1(2023)
• Page Start: 63
• Page End: 71
• Publication Date: 2023-01-31
• Subjects: Alzheimer's disease -- Aβ -- CNS infection -- herpes simplex virus (HSV) -- neuroinflammation -- varicella‐zoster virus (VZV); Brain; Neurosciences; Periodicals; 612.8
• DOI: 10.1002/ibra.12090
• Languages: English
• ISSNs: 2313-1934

Abstract

Abstract: Despite decades of repeated and intense research, the etiology of sudden Alzheimer's disease (AD) symptoms is still unclear. AD progressive pathology mainly involves neuron damage, depositions of amyloid‐beta (Aβ), and hyperphosphorylated tau protein. All these defects are manifested by exaggerated cytokine storm and neuroinflammation leading to irreversible brain damage in the long term. Despite the numerous risks and drawbacks associated with AD, it is believed that there is a hidden unknown causative and predisposing factors for AD. Extracellular vesicles (EVs) are small vesicles released by cells as a type of intercellular communication. Several pieces of evidence support the inclusion of viral components within EVs facilitating their penetration into the blood–brain barrier leading to neuroinflammation. In light of the SARS‐CoV‐19 pandemic and its related neurological complications, it is mandatory to highlight the possibility and viability of viral infections such as varicella‐zoster virus (VZV) and herpes simplex virus (HSV) on the onset of AD. Herein, the author is investigating the potential role of VZV and HSV along with highlighting the suggested route of pathogenesis entry resulting in AD manifestations. Additionally, this review aims to summarize the role of EVs in mediating the central nervous system viral infections leading to AD. Abstract : In the current study, we are highlighting the emerging mechanism of viral infections in Alzheimer's disease. Once infiltrated viral infection reaches the central nervous system via penetrating the blood–brain barrier, it directly results in a direct shift from resting microglia phenotype to reactive M1 microglia phenotype. The activation of microglia M1 phenotype cells triggers the release of inflammatory cytokines and mediators resulting in severe brain damage. This leads to exaggerated neurotoxins formation which results in neuroinflammation ending with tau protein and Aβ plaque depositions. Thus, viral infection may be considered a key pathogenic predisposing factor in the development of sudden Alzheimer's disease.