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Exploiting microglial and peripheral immune cell crosstalk to treat Alzheimer's disease
Dionisio-Santos DA, Olschowka JA, O'Banion MK.. Journal of neuroinflammation, 2019-04-05
Topic: Amyloid, tau and blood-test diagnosis
Neuroinflammation is considered one of the cardinal features of Alzheimer's disease (AD). Neuritic plaques composed of amyloid β and neurofibrillary tangle-laden neurons are surrounded by reactive astrocytes and microglia. Exposure of microglia, the resident myeloid cell of the CNS, to amyloid β causes these cells to acquire an inflammatory phenotype. While these reactive microglia are important to contain and phagocytose amyloid plaques, their activated phenotype impacts CNS homeostasis. In rodent models, increased neuroinflammation promoted by overexpression of proinflammatory cytokines can cause an increase in hyperphosphorylated tau and a decrease in hippocampal function. The peripheral immune system can also play a detrimental or beneficial role in CNS inflammation. Systemic inflammation can increase the risk of developing AD dementia, and chemokines released directly by microglia or indirectly by endothelial cells can attract monocytes and T lymphocytes to the CNS. These peripheral immune cells can aid in amyloid β clearance or modulate microglia responses, depending on the cell type. As such, several groups have targeted the peripheral immune system to modulate chronic neuroinflammation. In this review, we focus on the interplay of immunomodulating factors and cell types that are being investigated as possible therapeutic targets for the treatment or prevention of AD.
Key findings
- The peripheral immune system can also play a detrimental or beneficial role in CNS inflammation.
- Systemic inflammation can increase the risk of developing AD dementia, and chemokines released directly by microglia or indirectly by endothelial cells can attract monocytes and T lymphocytes to the CNS.
- These peripheral immune cells can aid in amyloid β clearance or modulate microglia responses, depending on the cell type.
- As such, several groups have targeted the peripheral immune system to modulate chronic neuroinflammation.
- In this review, we focus on the interplay of immunomodulating factors and cell types that are being investigated as possible therapeutic targets for the treatment or prevention of AD.
Why it matters
This review describes how the peripheral immune system can play a detrimental or beneficial role in brain inflammation and how several groups have targeted it as a possible therapeutic approach for Alzheimer's disease. These are investigated targets, not established treatments, and the review reports no proven cure or prevention.
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Study details
- Evidence strengthLow
How this study scored 48/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuroinflammation) |
| Journal's citation record | 2 / 4 | Journal of Neuroinflammation: journal h-index 216 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| 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 | 2019 — 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 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 184 times (OpenAlex, 2026-10-10) |
| Citations per year | 4 / 5 | 20.4 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 4 / 6 | Cited 9.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 6 other studies in this library |
| Still being cited | 2 / 4 | Cited 49 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author M. Kerry O’Banion: h-index 55 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Rochester: institution h-index 1,195 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30953557) |
| Free to read | 2 / 2 | Free to read |
| Total | 48 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s12974-019-1453-0
- PubMed: 30953557
- Original source →
- Free full text: Journal of Neuroinflammation →
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. Check the citation against the original before you use it.
APA 7th
Dionisio-Santos, D. A., Olschowka, J. A., & O'Banion, M. K. (2019). Exploiting microglial and peripheral immune cell crosstalk to treat Alzheimer's disease. Journal of neuroinflammation. https://doi.org/10.1186/s12974-019-1453-0
Vancouver
Dionisio-Santos DA, Olschowka JA, O'Banion MK. Exploiting microglial and peripheral immune cell crosstalk to treat Alzheimer's disease. Journal of neuroinflammation. 2019. doi:10.1186/s12974-019-1453-0. PMID: 30953557.
BibTeX
@article{dionisiosantos2019-30953557,
author = {Dionisio-Santos, D. A. and Olschowka, J. A. and O'Banion, M. K.},
title = {{Exploiting microglial and peripheral immune cell crosstalk to treat Alzheimer's disease}},
journal = {Journal of neuroinflammation},
year = {2019},
doi = {10.1186/s12974-019-1453-0},
pmid = {30953557},
url = {https://doi.org/10.1186/s12974-019-1453-0}
}
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