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Targeting Infectious Agents as a Therapeutic Strategy in Alzheimer's Disease
Fülöp T, Munawara U, Larbi A, Desroches M, Rodrigues S, Catanzaro M, Guidolin A, Khalil A et al.. CNS drugs, 2020-07-01
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is the most prevalent dementia in the world. Its cause(s) are presently largely unknown. The most common explanation for AD, now, is the amyloid cascade hypothesis, which states that the cause of AD is senile plaque formation by the amyloid β peptide, and the formation of neurofibrillary tangles by hyperphosphorylated tau. A second, burgeoning theory by which to explain AD is based on the infection hypothesis. Much experimental and epidemiological data support the involvement of infections in the development of dementia. According to this mechanism, the infection either directly or via microbial virulence factors precedes the formation of amyloid β plaques. The amyloid β peptide, possessing antimicrobial properties, may be beneficial at an early stage of AD, but becomes detrimental with the progression of the disease, concomitantly with alterations to the innate immune system at both the peripheral and central levels. Infection results in neuroinflammation, leading to, and sustained by, systemic inflammation, causing eventual neurodegeneration, and the senescence of the immune cells. The sources of AD-involved microbes are various body microbiome communities from the gut, mouth, nose, and skin. The infection hypothesis of AD opens a vista to new therapeutic approaches, either by treating the infection itself or modulating the immune system, its senescence, or the body's metabolism, either separately, in parallel, or in a multi-step way.
Key findings
- Infection results in neuroinflammation, leading to, and sustained by, systemic inflammation, causing eventual neurodegeneration, and the senescence of the immune cells.
Why it matters
This review lays out the infection hypothesis of Alzheimer's, in which microbes from the gut, mouth, nose or skin may come before amyloid β plaques and trigger neuroinflammation that leads to brain damage. The authors argue this opens new therapeutic approaches, such as treating the infection itself or modulating the immune system, which they put forward as directions rather than tested treatments.
Study details
- Study designsystematic review
- Evidence strengthLow
How this study scored 53/100
Published in a peer-reviewed journal, and it is a systematic review of all the studies on the question. Scored zero for sample size, effect reported and studied in people because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (CNS drugs) |
| Journal's citation record | 2 / 4 | CNS Drugs: journal h-index 164 (OpenAlex, 2026-10-29) |
| Study design | 12 / 12 | A systematic review of all the studies on the question |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2020 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | A review of other studies — randomisation is not credited here |
| Times cited | 3 / 7 | Cited 35 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.4 citations a year over 8 year(s) since 2020 |
| Impact for its field and year | 2 / 6 | Cited 2.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 2 / 4 | Cited 15 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Eric H. Frost: h-index 45 (OpenAlex, whole career) |
| Institution's track record | 3 / 3 | Stanford University: institution h-index 2,684 (OpenAlex) |
| Multi-centre collaboration | 3 / 3 | OpenAlex lists 15 institution(s) in 9 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 32458360) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 53 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1007/s40263-020-00737-1
- PubMed: 32458360
- Original source →
- Free full text: BIRD (Basque Center for Applied Mathematics) →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
APA 7th
Fülöp, T., Munawara, U., Larbi, A., Desroches, M., Rodrigues, S., Catanzaro, M., et al. (2020). Targeting Infectious Agents as a Therapeutic Strategy in Alzheimer's Disease. CNS drugs. https://doi.org/10.1007/s40263-020-00737-1
Vancouver
Fülöp T, Munawara U, Larbi A, Desroches M, Rodrigues S, Catanzaro M, et al. Targeting Infectious Agents as a Therapeutic Strategy in Alzheimer's Disease. CNS drugs. 2020. doi:10.1007/s40263-020-00737-1. PMID: 32458360.
BibTeX
@article{fulop2020-32458360,
author = {Fülöp, T. and Munawara, U. and Larbi, A. and Desroches, M. and Rodrigues, S. and Catanzaro, M. and Guidolin, A. and Khalil, A. and others},
title = {{Targeting Infectious Agents as a Therapeutic Strategy in Alzheimer's Disease}},
journal = {CNS drugs},
year = {2020},
doi = {10.1007/s40263-020-00737-1},
pmid = {32458360},
url = {https://doi.org/10.1007/s40263-020-00737-1}
}
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