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Locus ceruleus degeneration promotes Alzheimer pathogenesis in amyloid precursor protein 23 transgenic mice
Heneka MT, Ramanathan M, Jacobs AH, Dumitrescu-Ozimek L, Bilkei-Gorzo A, Debeir T, Sastre M, Galldiks N et al.. The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006-02-01
Topic: Brain proteins, microglia and lab models
Locus ceruleus (LC) degeneration and loss of cortical noradrenergic innervation occur early in Alzheimer's disease (AD). Although this has been known for several decades, the contribution of LC degeneration to AD pathogenesis remains unclear. We induced LC degeneration with N-(2-chloroethyl)-N-ethyl-bromo-benzylamine (dsp4) in amyloid precursor protein 23 (APP23) transgenic mice with a low amyloid load.
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APA 7th
Heneka, M. T., Ramanathan, M., Jacobs, A. H., Dumitrescu-Ozimek, L., Bilkei-Gorzo, A., Debeir, T., et al. (2006). Locus ceruleus degeneration promotes Alzheimer pathogenesis in amyloid precursor protein 23 transgenic mice. The Journal of neuroscience : the official journal of the Society for Neuroscience. https://doi.org/10.1523/jneurosci.4236-05.2006
Vancouver
Heneka MT, Ramanathan M, Jacobs AH, Dumitrescu-Ozimek L, Bilkei-Gorzo A, Debeir T, et al. Locus ceruleus degeneration promotes Alzheimer pathogenesis in amyloid precursor protein 23 transgenic mice. The Journal of neuroscience : the official journal of the Society for Neuroscience. 2006. doi:10.1523/jneurosci.4236-05.2006. PMID: 16452658.
BibTeX
@article{heneka2006-16452658,
author = {Heneka, M. T. and Ramanathan, M. and Jacobs, A. H. and Dumitrescu-Ozimek, L. and Bilkei-Gorzo, A. and Debeir, T. and Sastre, M. and Galldiks, N. and others},
title = {{Locus ceruleus degeneration promotes Alzheimer pathogenesis in amyloid precursor protein 23 transgenic mice}},
journal = {The Journal of neuroscience : the official journal of the Society for Neuroscience},
year = {2006},
doi = {10.1523/jneurosci.4236-05.2006},
pmid = {16452658},
url = {https://doi.org/10.1523/jneurosci.4236-05.2006}
}
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.
Key findings
- Although this has been known for several decades, the contribution of LC degeneration to AD pathogenesis remains unclear.
- We induced LC degeneration with N-(2-chloroethyl)-N-ethyl-bromo-benzylamine (dsp4) in amyloid precursor protein 23 (APP23) transgenic mice with a low amyloid load.
- Then 6 months later the LC projection areas showed a robust elevation of glial inflammation along with augmented amyloid plaque deposits.
- Moreover, neurodegeneration and neuronal loss significantly increased.
Why it matters
In APP23 transgenic mice, damaging the locus ceruleus led six months later to more glial inflammation, more amyloid plaques, and greater neurodegeneration and neuronal loss. This is animal evidence that locus ceruleus degeneration may contribute to Alzheimer's progression, not a proven treatment for people.
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Study details
- Evidence strengthLow
How this study scored 47/100
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 (The Journal of neuroscience : the official journal of the Society for 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 | 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 | 2006 — older than 20 years, still counted |
| 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 “transgenic”) — 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 304 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 13.8 citations a year over 22 year(s) since 2006 |
| Impact for its field and year | 3 / 6 | Cited 6.5× 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 35 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Matthias Staufenbiel: h-index 95 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Max Planck Society: institution h-index 1,183 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 6 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 16452658) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 47 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1523/jneurosci.4236-05.2006
- PubMed: 16452658
- Original source →
- Free full text: Journal of Neuroscience →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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