Time to test antibacterial therapy in Alzheimer’s disease
Open accessAbstract
Alzheimer’s disease is associated with cerebral accumulation of amyloid-β peptide and hyperphosphorylated tau. In the past 28 years, huge efforts have been made in attempting to treat the disease by reducing brain accumulation of amyloid-β in patients with Alzheimer’s disease, with no success. While anti-amyloid-β therapies continue to be tested in prodromal patients with Alzheimer’s disease and in subjects at risk of developing Alzheimer’s disease, there is an urgent need to provide therapeutic support to patients with established Alzheimer’s disease for whom current symptomatic treatment (acetylcholinesterase inhibitors and N-methyl d-aspartate antagonist) provide limited help. The possibility of an infectious aetiology for Alzheimer’s disease has been repeatedly postulated over the past three decades. Infiltration of the brain by pathogens may act as a trigger or co-factor for Alzheimer’s disease, with Herpes simplex virus type 1, Chlamydia pneumoniae, and Porphyromonas gingivalis being most frequently implicated. These pathogens may directly cross a weakened blood–brain barrier, reach the CNS and cause neurological damage by eliciting neuroinflammation. Alternatively, pathogens may cross a weakened intestinal barrier, reach vascular circulation and then cross blood–brain barrier or cause low grade chronic inflammation and subsequent neuroinflammation from the periphery. The gut microbiota comprises a complex community of microorganisms. Increased permeability of the gut and blood–brain barrier induced by microbiota dysbiosis may impact Alzheimer’s disease pathogenesis. Inflammatory microorganisms in gut microbiota are associated with peripheral inflammation and brain amyloid-β deposition in subjects with cognitive impairment. Oral microbiota may also influence Alzheimer’s disease risk through circulatory or neural access to the brain. At least two possibilities can be envisaged to explain the association of suspected pathogens and Alzheimer’s disease. One is that patients with Alzheimer’s disease are particularly prone to microbial infections. The other is that microbial infection is a contributing cause of Alzheimer’s disease. Therapeutic trials with antivirals and/or antibacterials could resolve this dilemma. Indeed, antiviral agents are being tested in patients with Alzheimer’s disease in double-blind placebo-controlled studies. Although combined antibiotic therapy was found to be effective in animal models of Alzheimer’s disease, antibacterial drugs are not being widely investigated in patients with Alzheimer’s disease. This is because it is not clear which bacterial populations in the gut of patients with Alzheimer’s disease are overexpressed and if safe, selective antibacterials are available for them. On the other hand, a bacterial protease inhibitor targeting P. gingivalis toxins is now being tested in patients with Alzheimer’s disease. Clinical studies are needed to test if countering bacterial infection may be beneficial in patients with established Alzheimer’s disease.
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Viruses such as herpes viruses, cytomegalovirus, HIV, VZV, EBV, and Hepatitis C virus have been implicated in Alzheimer's disease pathogenesis.
“Viruses, such as herpes viruses, cytomegalovirus, human immunodeficiency virus (HIV), Varicela zoster virus (VZV), Epstein–Barr virus (EBV), and Hepatitis C virus, have been implicated in Alzheimer’s disease pathogenesis [7, 10].”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [10]
According to the viral hypothesis of AD, the interaction between viral presence and AD may be non-specifically associated with up-regulation of inflammatory responses and oxidative stress.
“According to the ‘viral hypothesis of AD’, this interaction may be non-specifically associated with up-regulation of inflammatory responses and oxidative stress, which are secondary, but relevant components of the amyloid cascade.”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [10]
The interaction between viral presence and AD may also operate through a specific mechanism within the core pathogenesis, hastening amyloid overproduction.
“This interaction may also operate through a specific mechanism within the core pathogenesis, hastening amyloid overproduction [10, 12].”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [10]
Viral presence in the CNS may interfere with pathogenic mechanisms related to neurodegenerative diseases, such as Alzheimer's disease.
“Viral presence in the CNS may interfere with pathogenic mechanisms related to neurodegenerative diseases, such as Alzheimer’s disease (AD) [7, 10].”
From Cognitive decline following acute viral infections: literature review and projections for post-COVID-19 (2022) · cites this paper as [10]
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- Authors
- Panza, F., Lozupone, M., Solfrizzi, V., Watling, M., & Imbimbo, B. P.
- Affiliations
- Gastroenterology Hospital "Saverio de Bellis" (IT)
- University of Bari Aldo Moro (IT)
- Chiesi (Italy) (IT)
- Corresponding author
- Panza, Francesco
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2019-08-29
- Volume
- 142
- Issue
- 10
- Pages
- 2905-2929
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- OpenAlex
- W2973900732
- Cited by
- 161
- References
- 258
- Citations by year
- 2026: 4 · 2025: 19 · 2024: 19 · 2023: 23 · 2022: 28 · 2021: 39 · 2020: 26 · 2019: 3
- FWCI
- 2.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Brain (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion, cc-by-nc-nd)
- Funders
- Fondazione Dieta Mediterranea
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, antibiotic therapy, amyloid-beta, tau hyperphosphorylation, infectious etiology, neuroinflammation, blood-brain barrier, gut microbiota, dysbiosis, gut-brain axis, Porphyromonas gingivalis, Chlamydia pneumoniae, herpes simplex virus type 1, antiviral therapy
- MeSH terms
- Gastrointestinal Microbiome, Alzheimer Disease, Animals, Anti-Bacterial Agents, Brain, Disease Models, Animal, Double-Blind Method, Humans, Inflammation, Placebos, Neuroimmunomodulation, Amyloid beta-Peptides, Cognitive Dysfunction, Microbiota
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