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Chronic low-dose-rate ionising radiation affects the hippocampal phosphoproteome in the ApoE-/- Alzheimer's mouse model
Kempf SJ, Janik D, Barjaktarovic Z, Braga-Tanaka I, Tanaka S, Neff F, Saran A, Larsen MR et al.. Oncotarget, 2016-11-01
Topic: Brain proteins, microglia and lab models
Accruing data indicate that radiation-induced consequences resemble pathologies of neurodegenerative diseases such as Alzheimer´s. The aim of this study was to elucidate the effect on hippocampus of chronic low-dose-rate radiation exposure (1 mGy/day or 20 mGy/day) given over 300 days with cumulative doses of 0.3 Gy and 6.0 Gy, respectively. ApoE deficient mutant C57Bl/6 mouse was used as an Alzheimer´s model. Using mass spectrometry, a marked alteration in the phosphoproteome was found at both dose rates. The radiation-induced changes in the phosphoproteome were associated with the control of synaptic plasticity, calcium-dependent signalling and brain metabolism. An inhibition of CREB signalling was found at both dose rates whereas Rac1-Cofilin signalling was found activated only at the lower dose rate. Similarly, the reduction in the number of activated microglia in the molecular layer of hippocampus that paralleled with reduced levels of TNFα expression and lipid peroxidation was significant only at the lower dose rate. Adult neurogenesis, investigated by Ki67, GFAP and NeuN staining, and cell death (activated caspase-3) were not influenced at any dose or dose rate. This study shows that several molecular targets induced by chronic low-dose-rate radiation overlap with those of Alzheimer´s pathology. It may suggest that ionising radiation functions as a contributing risk factor to this neurodegenerative disease.
Key findings
- Accruing data indicate that radiation-induced consequences resemble pathologies of neurodegenerative diseases such as Alzheimer´s.
- The radiation-induced changes in the phosphoproteome were associated with the control of synaptic plasticity, calcium-dependent signalling and brain metabolism.
- Similarly, the reduction in the number of activated microglia in the molecular layer of hippocampus that paralleled with reduced levels of TNFα expression and lipid peroxidation was significant only at the lower dose rate.
- It may suggest that ionising radiation functions as a contributing risk factor to this neurodegenerative disease.
Why it matters
In an Alzheimer's mouse model, chronic low-dose-rate radiation changed the hippocampal phosphoproteome in ways that overlapped with Alzheimer's pathology, including inhibition of CREB signalling. This is animal work suggesting radiation may be a contributing risk factor, and it does not test any treatment, cure or prevention for people.
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Study details
- Evidence strengthLow
How this study scored 39/100
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 (Oncotarget) |
| Journal's citation record | 2 / 4 | Oncotarget: journal h-index 222 (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 | 2016 — 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 “mouse”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 48 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.0 citations a year over 12 year(s) since 2016 |
| Impact for its field and year | 2 / 6 | Cited 3.0× 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 | 1 / 4 | Cited 10 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 2 / 4 | Last-listed author Soile Tapio: h-index 42 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Helmholtz Munich: institution h-index 892 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 4 institution(s) in 4 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 27708245) |
| Free to read | 2 / 2 | Free to read |
| Total | 39 / 100 | — |
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Read the original
Full text: free to read — PubMed Central lists this copy as free to read: the link above (checked 10 Oct 2026).
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
Kempf, S. J., Janik, D., Barjaktarovic, Z., Braga-Tanaka, I., Tanaka, S., Neff, F., et al. (2016). Chronic low-dose-rate ionising radiation affects the hippocampal phosphoproteome in the ApoE-/- Alzheimer's mouse model. Oncotarget. https://doi.org/10.18632/oncotarget.12376
Vancouver
Kempf SJ, Janik D, Barjaktarovic Z, Braga-Tanaka I, Tanaka S, Neff F, et al. Chronic low-dose-rate ionising radiation affects the hippocampal phosphoproteome in the ApoE-/- Alzheimer's mouse model. Oncotarget. 2016. doi:10.18632/oncotarget.12376. PMID: 27708245.
BibTeX
@article{kempf2016-27708245,
author = {Kempf, S. J. and Janik, D. and Barjaktarovic, Z. and Braga-Tanaka, I. and Tanaka, S. and Neff, F. and Saran, A. and Larsen, M. R. and others},
title = {{Chronic low-dose-rate ionising radiation affects the hippocampal phosphoproteome in the ApoE-/- Alzheimer's mouse model}},
journal = {Oncotarget},
year = {2016},
doi = {10.18632/oncotarget.12376},
pmid = {27708245},
url = {https://doi.org/10.18632/oncotarget.12376}
}
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