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57/100

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Inflammation and the immune system

Topic: Amyloid, tau and blood-test diagnosis

Early microglial accumulation in Alzheimer's disease (AD) delays disease progression by promoting clearance of beta-amyloid (Abeta) before formation of senile plaques. However, persistent Abeta accumulation despite increasing microglial numbers suggests that the ability of microglia to clear Abeta may decrease with age and progression of AD pathology. To determine the effects of aging and Abeta deposition on microglial ability to clear Abeta, we used quantitative PCR to analyze gene expression in freshly isolated adult microglia from 1.5-, 3-, 8-, and 14-month-old transgenic PS1-APP mice, an established mouse model of AD, and from their nontransgenic littermates. We found that microglia from old PS1-APP mice, but not from younger mice, have a twofold to fivefold decrease in expression of the Abeta-binding scavenger receptors scavenger receptor A (SRA), CD36, and RAGE (receptor for advanced-glycosylation endproducts), and the Abeta-degrading enzymes insulysin, neprilysin, and MMP9, compared with their littermate controls. In contrast, PS1-APP microglia had a 2.5-fold increase in the proinflammatory cytokines IL-1beta (interleukin-1beta) and tumor necrosis factor alpha (TNFalpha), suggesting that there is an inverse correlation between cytokine production and Abeta clearance. In support of this possibility, we found that incubation of cultured N9 mouse microglia with TNFalpha decreased the expression of SRA and CD36 and reduced Abeta uptake. Our data indicate that, although early microglial recruitment promotes Abeta clearance and is neuroprotective in AD, as disease progresses, proinflammatory cytokines produced in response to Abeta deposition downregulate genes involved in Abeta clearance and promote Abeta accumulation, therefore contributing to neurodegeneration. Antiinflammatory therapy for AD should take this dichotomous microglial role into consideration.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Hickman, S. E., Allison, E. K., & El Khoury, J. B. (2008). Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice. Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0616-08.2008

Vancouver

Hickman SE, Allison EK, El Khoury JB. Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice. Journal of Neuroscience. 2008. doi:10.1523/jneurosci.0616-08.2008. PMID: 18701698.

BibTeX

@article{hickman2008-18701698,
  author  = {Hickman, Suzanne E. and Allison, Elizabeth K. and El Khoury, Joseph B.},
  title   = {{Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice}},
  journal = {Journal of Neuroscience},
  year    = {2008},
  doi     = {10.1523/jneurosci.0616-08.2008},
  pmid    = {18701698},
  url     = {https://doi.org/10.1523/jneurosci.0616-08.2008}
}

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.

Why it matters

In a mouse model of Alzheimer's disease, microglia from old mice had lower expression of genes that bind and break down amyloid-β than those from littermate controls, and higher levels of inflammatory cytokines. The authors suggest that as disease progresses, these cytokines turn down amyloid clearance genes and promote amyloid build-up.

How this study scored 57/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on strength of evidence, so that was left out: it earned 54 of the 95 points we could judge it on, which is 57 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of Neuroscience)
Journal's citation record	4 / 4	Journal of Neuroscience: journal h-index 651 (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	— / 5	No evidence rating recorded — left out of this score
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	1 / 5	2008 — within 20 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	Laboratory or animal study (title names “mice”) — scores zero
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	7 / 7	Cited 1,326 times (OpenAlex, 2026-10-10)
Citations per year	5 / 5	66.3 citations a year over 20 year(s) since 2008
Impact for its field and year	5 / 6	Cited 23.7× 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	4 / 4	Cited 213 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Joseph B. El Khoury: h-index 51 (OpenAlex, whole career)
Institution's track record	3 / 3	Harvard University: institution h-index 3,235 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 18701698)
Free to read	2 / 2	Free to read
Points	54 / 95	Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 54 of the 95 points we could judge it on is 57 out of 100.
Total	57 / 100	—

What each of these 20 components measures, and what this score is not →

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