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High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice
Thirumangalakudi L, Prakasam A, Zhang R, Bimonte-Nelson H, Sambamurti K, Kindy MS, Bhat NR.. Journal of neurochemistry, 2008-07-01
Topic: Brain proteins, microglia and lab models
Recent findings suggest that hypercholesterolemia may contribute to the onset of Alzheimer's disease-like dementia but the underlying mechanisms remain unknown. In this study, we evaluated the cognitive performance in rodent models of hypercholesterolemia in relation to neuroinflammatory changes and amyloid precursor protein (APP) processing, the two key parameters of Alzheimer's disease pathogenesis. Groups of normal C57BL/6 and low density lipoprotein receptor (LDLR)-deficient mice were fed a high fat/cholesterol diet for an 8-week period and tested for memory in a radial arm maze.
Key findings
- In this study, we evaluated the cognitive performance in rodent models of hypercholesterolemia in relation to neuroinflammatory changes and amyloid precursor protein (APP) processing, the two key parameters of Alzheimer's disease pathogenesis.
- Groups of normal C57BL/6 and low density lipoprotein receptor (LDLR)-deficient mice were fed a high fat/cholesterol diet for an 8-week period and tested for memory in a radial arm maze.
- It was found that the C57BL/6 mice receiving a high fat diet were deficient in handling an increasing working memory load compared with counterparts receiving a control diet while the hypercholesterolemic LDLR-/- mice showed impaired working memory regardless of diet.
- Immunohistochemical analysis revealed the presence of activated microglia and astrocytes in the hippocampi from high fat-fed C57BL/6 mice and LDLR-/- mice.
Why it matters
In mice fed a high fat/cholesterol diet, memory loss was found to correlate with neuroinflammatory changes and altered amyloid precursor protein processing. This is animal work, so it does not show that lowering cholesterol in people prevents or treats Alzheimer's disease.
Study details
- Evidence strengthLow
How this study scored 45/100
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.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neurochemistry) |
| Journal's citation record | 3 / 4 | Journal of Neurochemistry: journal h-index 349 (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 | 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 | 6 / 7 | Cited 361 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 18.1 citations a year over 20 year(s) since 2008 |
| Impact for its field and year | 4 / 6 | Cited 8.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 2 / 6 | Cited by 5 other studies in this library |
| Still being cited | 2 / 4 | Cited 45 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Narayan R. Bhat: h-index 41 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Arizona State University: institution h-index 987 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 18410513) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 45 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1111/j.1471-4159.2008.05415.x
- PubMed: 18410513
- Original source →
- Free full text: PubMed Central →
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 names 7 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
APA 7th
Thirumangalakudi, L., Prakasam, A., Zhang, R., Bimonte-Nelson, H., Sambamurti, K., Kindy, M. S., et al. (2008). High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice. Journal of neurochemistry. https://doi.org/10.1111/j.1471-4159.2008.05415.x
Vancouver
Thirumangalakudi L, Prakasam A, Zhang R, Bimonte-Nelson H, Sambamurti K, Kindy MS, et al. High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice. Journal of neurochemistry. 2008. doi:10.1111/j.1471-4159.2008.05415.x. PMID: 18410513.
BibTeX
@article{thirumangalakudi2008-18410513,
author = {Thirumangalakudi, L. and Prakasam, A. and Zhang, R. and Bimonte-Nelson, H. and Sambamurti, K. and Kindy, M. S. and Bhat, N. R.},
title = {{High cholesterol-induced neuroinflammation and amyloid precursor protein processing correlate with loss of working memory in mice}},
journal = {Journal of neurochemistry},
year = {2008},
doi = {10.1111/j.1471-4159.2008.05415.x},
pmid = {18410513},
url = {https://doi.org/10.1111/j.1471-4159.2008.05415.x}
}
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