Cited by 34Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Activation of Endogenous Retrovirus, Brain Infections and Environmental Insults in Neurodegeneration and Alzheimer’s Disease

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Licastro, Federico, Porcellini, Elisa·2021·International Journal of Molecular Sciences

Abstract

Chronic neurodegenerative diseases are complex, and their pathogenesis is uncertain. Alzheimer’s disease (AD) is a neurodegenerative brain alteration that is responsible for most dementia cases in the elderly. AD etiology is still uncertain; however, chronic neuroinflammation is a constant component of brain pathology. Infections have been associated with several neurological diseases and viruses of the Herpes family appear to be a probable cause of AD neurodegenerative alterations. Several different factors may contribute to the AD clinical progression. Exogeneous viruses or other microbes and environmental pollutants may directly induce neurodegeneration by activating brain inflammation. In this paper, we suggest that exogeneous brain insults may also activate retrotransposons and silent human endogenous retroviruses (HERVs). The initial inflammation of small brain areas induced by virus infections or other brain insults may activate HERV dis-regulation that contributes to neurodegenerative mechanisms. Chronic HERV activation in turn may cause progressive neurodegeneration that thereafter merges in cognitive impairment and dementia in genetically susceptible people. Specific treatment for exogenous end endogenous pathogens and decreasing pollutant exposure may show beneficial effect in early intervention protocol to prevent the progression of cognitive deterioration in the elderly.

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  • HSV infection-induced persistent inflammation leads to Aβ peptide overproduction and aggregation.

    “As a result, HSV infection-induced persistent inflammation leads to Aβ peptide overproduction and aggregation.101”

    From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [101]

    Section 2 says persistent or latent herpesvirus infection may lead to Aβ overproduction and amyloid plaque formation. Section 5.1 reports increased Aβ after HSV-1 infection and describes amyloid accumulation alongside neuroinflammation in a mouse model. Neither section establishes that persistent inflammation is the mechanism causing Aβ overproduction and aggregation; the claim also states a tentative link as a definite one. Page numbers were not available in our copy. (LLM, conf=0.86)

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Authors
Licastro, F., & Porcellini, E.
Affiliations
University of Bologna (IT)
Corresponding author
Licastro, Federico
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2021-07-06
Volume
22
Issue
14
Pages
7263
ISSN
1422-0067 (ISSN-L)
OpenAlex
W3179758880
Cited by
33
References
98
Citations by year
2026: 3 · 2025: 11 · 2024: 4 · 2023: 3 · 2022: 10 · 2021: 2
FWCI
0.63
Type
journal article
Language
en
Open access
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Alzheimer's disease, endogenous retroviruses, retrotransposons, neuroinflammation, brain infection, herpesvirus, environmental pollutants, neurodegeneration, dementia, cognitive impairment
MeSH terms
Alzheimer Disease, Animals, Brain, Cognition Disorders, Encephalitis, Humans, Virus Diseases, Endogenous Retroviruses

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