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Infections, Inflammation and Neurodegeneration in Alzheimer’s Disease 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 4263

Special Issue Editor


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Guest Editor
Department of Experimental, Diagnostic, Specialty Medicine School of Medicine University of Bologna, Bologna, Italy
Interests: genetic and environmental AD risk factors; brain immune mechanisms; virus infections; AD prevention; predictive medicine; AD risk; chart; personalized AD risk assessment
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Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is the most common neurodegenerative disorder. With the rapid advancement of gene typing technologies and genome-wide association studies, several AD risk genes have so far been identified and confirmed, including CLU, CR1, PICALM, SORL1, TREM2, and CD33. However, apart from APOE polymorphism, each gene has a limited OR for AD. It is of interest that all these genes are involved in different immune responses against pathogens.

Microbes are emerging risk factors for the disease and substantial new data have been recently published supporting the general hypothesis that virus, some bacteria, and fungi appear to be associated with the clinical history of dementia. Moreover, infections may also be involved in brain inflammation and some aspects of neurodegeneration associated with AD.

As volume 1 of the Special Issue “Infections, Inflammation and Neurodegeneration in Alzheimer's Disease” has been successful, we will be exploring this issue further in the International Journal of Molecular Sciences (ISSN 1422-0067, IF 5.924, JCR Category Q1). In this second Special Issue, the main topic will be infections, inflammation and neuro-degeneration in Alzheimer's disease. It is dedicated to research articles and reviews regarding infectious agents associated with AD, immune mechanisms involved in the brain defenses, inflammatory processes, and neuro-pathological markers of AD. The emphasis will be on novel AD-related mechanism of infections, brain reaction to these invaders and the brain and systemic inflammatory responses against brain AD-related pathogens and their involvement in neurodegenerative mechanisms. New insights for infection diagnosis, identification of potential pathogenic pathways, therapeutic and preventive measures and vaccination are the focus of this Special Issue of the International Journal of Molecular Sciences.

Dr. Federico Licastro
Guest Editor

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Keywords

  • virus, bacterial and fungal infections
  • AD pathogenesis and CNS and peripheral inflammation
  • amyloid peptides
  • brain amyloid and anti-microorganism defense
  • gene signature and brain infections
  • APOE gene and infections
  • dementia and anti-infective therapy
  • vaccination and AD
  • risk factors and dementia prevention.

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Published Papers (1 paper)

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Research

21 pages, 6010 KiB  
Article
Intracerebral but Not Peripheral Infection of Live Porphyromonas gingivalis Exacerbates Alzheimer’s Disease Like Amyloid Pathology in APP-TgCRND8 Mice
by Chairmandurai Aravindraja, Ravi Sakthivel, Xuefei Liu, Marshall Goodwin, Patnam Veena, Valentina Godovikova, J. Christopher Fenno, Yona Levites, Todd E. Golde and Lakshmyya Kesavalu
Int. J. Mol. Sci. 2022, 23(6), 3328; https://doi.org/10.3390/ijms23063328 - 19 Mar 2022
Cited by 9 | Viewed by 3916
Abstract
The impact of oral microbial dysbiosis on Alzheimer’s disease (AD) remains controversial. Building off recent studies reporting that various microbes might directly seed or promote amyloid β (Aβ) deposition, we evaluated the effects of periodontal bacteria (Porphyromonas gingivalis, Treponema denticola) and supragingival [...] Read more.
The impact of oral microbial dysbiosis on Alzheimer’s disease (AD) remains controversial. Building off recent studies reporting that various microbes might directly seed or promote amyloid β (Aβ) deposition, we evaluated the effects of periodontal bacteria (Porphyromonas gingivalis, Treponema denticola) and supragingival commensal (Streptococcus gordonii) oral bacterial infection in the APP-transgenic CRND8 (Tg) mice model of AD. We tracked bacterial colonization and dissemination, and monitored effects on gliosis and amyloid deposition. Chronic oral infection did not accelerate Aβ deposition in Tg mice but did induce alveolar bone resorption, IgG immune response, and an intracerebral astrogliosis (GFAP: glial fibrillary acidic protein). In contrast, intracerebral inoculation of live but not heat-killed P. gingivalis increased Aβ deposition and Iba-1 (ionized calcium-binding adaptor-1) microgliosis after 8 weeks of bacterial infection but not at 4 days. These data show that there may be differential effects of infectious microbes on glial activation and amyloid deposition depending on the species and route of inoculation, and thereby provide an important framework for future studies. Indeed, these studies demonstrate marked effects on amyloid β deposition only in a fairly non-physiologic setting where live bacteria is injected directly into the brain. Full article
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