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Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
Published on: December 26, 2016
Persistent infections, immune-senescence and Alzheimer's disease
Federico Licastro1, Elisa Porcellini1
1Department of Experimental, Diagnostic and Specialty Medicine, School of Medicine, University of Bologna, Bologna 40126, Italy.
Abstract:
Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia. Classical hallmarks of AD such as amyloid deposition and neurofibrillary tangles do not completely explain AD pathogenesis. Recent investigations proposed Aβ peptide as an anti-microbial factor. Our previous works suggested that the concomitant presence of single nucleotide polymorphisms (SNPs) from AD genetic studies might impair antiviral defenses and increase the individual susceptibility to herpes virus infection. Viruses of herpes family by inducing frequent cycles of reactivation and latency constantly challenge the immune response and drive the accumulation of memory T cells. However, the immune system is not able to completely eradicate these viruses. The continuous antigen stimulation activates chronic inflammatory responses that may progressively induce neurodegenerative mechanisms in genetically susceptible elderly. The aim of this paper is to suggest new perspectives in clinical pathogenesis of AD with potential prevention and new medical treatment of the age associated cognitive decline.
Insights
Alzheimer's disease may be linked to herpes virus infections, especially in genetically susceptible individuals. This challenges the immune system, potentially leading to neurodegeneration and cognitive decline.
Area of Science:
- Neuroscience
- Immunology
- Infectious Disease
Background:
- Alzheimer's disease (AD) is a leading cause of dementia, but its exact pathogenesis remains incompletely understood.
- Classical hallmarks like amyloid plaques and neurofibrillary tangles do not fully explain AD.
- Emerging research suggests Aβ peptides may have antimicrobial functions, and herpes viruses are implicated in AD.
Discussion:
- Genetic factors, specifically single nucleotide polymorphisms (SNPs), may compromise antiviral defenses, increasing susceptibility to herpes virus infections.
- Herpes viruses, through cycles of latency and reactivation, continuously stimulate the immune system, promoting chronic inflammation.
- This sustained immune activation in genetically susceptible elderly individuals may drive progressive neurodegenerative mechanisms.
Key Insights:
- A novel perspective links herpes virus infections and genetic predispositions to Alzheimer's disease pathogenesis.
- Chronic immune stimulation by persistent viral infections could be a key factor in neurodegeneration.
- This hypothesis offers a new framework for understanding AD beyond traditional hallmarks.
Outlook:
- Exploring the interplay between genetics, viral infections, and immune responses in AD.
- Developing new preventative strategies and medical treatments targeting viral infections and inflammation for age-associated cognitive decline.
- Investigating the potential of antiviral therapies for Alzheimer's disease prevention and treatment.
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