IMR Press / JIN / Volume 21 / Issue 2 / DOI: 10.31083/j.jin2102073
Open Access Review
Infectious agents and Alzheimer's disease
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1 Laboratory of Neurobiology, Department of Neurology, Poznan University of Medical Sciences, 60-355 Poznan, Poland
2 Chair and Department of Neurology, Poznan University of Medical Sciences, 60-355 Poznan, Poland
*Correspondence:; (Jolanta Dorszewska)
Academic Editor: Rafael Franco
J. Integr. Neurosci. 2022, 21(2), 73;
Submitted: 8 March 2021 | Revised: 25 March 2021 | Accepted: 29 April 2021 | Published: 28 March 2022
(This article belongs to the Special Issue Neurodegeneration and neuroinflammation)
Copyright: © 2022 The Author(s). Published by IMR Press.
This is an open access article under the CC BY 4.0 license.

Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Individuals affected by the disease gradually lose their capacity for abstract thinking, understanding, communication and memory. As populations age, declining cognitive abilities will represent an increasing global health concern. While AD was first described over a century ago, its pathogenesis remains to be fully elucidated. It is believed that cognitive decline in AD is caused by a progressive loss of neurons and synapses that lead to reduced neural plasticity. AD is a multifactorial disease affected by genetic and environmental factors. The molecular hallmarks of AD include formation of extracellular β amyloid (Aβ) aggregates, neurofibrillary tangles of hyperphosphorylated tau protein, excessive oxidative damage, an imbalance of biothiols, dysregulated methylation, and a disproportionate inflammatory response. Recent reports have shown that viruses (e.g., Herpes simplex type 1, 2, 6A/B; human cytomegalovirus, Epstein-Barr virus, hepatitis C virus, influenza virus, and severe acute respiratory syndrome coronavirus 2, SARS-CoV-2), bacteria (e.g., Treponema pallidum, Borrelia burgdorferi, Chlamydia pneumoniae, Porphyromonas gingivalis, Prevotella intermedia, Tannerella forsythia, Fusobacterium nucleatum, Aggregatibacter actinomycetemcmitans, Eikenella corrodens, Treponema denticola, and Helicobacter pylori), as well as eukaryotic unicellular parasites (e.g., Toxoplasma gondii) may factor into cognitive decline within the context of AD. Microorganisms may trigger pathological changes in the brain that resemble and/or induce accumulation of Aβ peptides and promote tau hyperphosphorylation. Further, the mere presence of infectious agents is suspected to induce both local and systemic inflammatory responses promoting cellular damage and neuronal loss.

Here we review the influence of infectious agents on the development of AD to inspire new research in dementia based on these pathogens.

Alzheimer's disease
Cognitive decline
Infectious agents
Fig. 1.
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