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Caloric restriction attenuates amyloid deposition in middle-aged dtg APP/PS1 mice
Mouton PR, Chachich ME, Quigley C, Spangler E, Ingram DK.. Neuroscience letters, 2009-08-20
Topic: Brain proteins, microglia and lab models
Caloric restriction (CR) mitigates neurological damage arising from aging and a variety of other sources, including neuropathology in young adult mice that express single and double transgenic (tg) mutations associated with Alzheimer disease (AD). To evaluate the potential of CR to protect against relatively heavy AD-type pathology, middle-aged (13-14-month-old) mice that co-express two mutations related to familial AD, amyloid precursor protein (APP) and presenilin 1 (PS1), were fed balanced diets with 40% fewer calories than ad libitum-fed controls. Following 18 weeks of treatment, mice were killed and brains were processed for quantification of total volume of amyloid-beta (Abeta) in the hippocampal formation and the overlying neocortex.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Mouton, P. R., Chachich, M. E., Quigley, C., Spangler, E., & Ingram, D. K. (2009). Caloric restriction attenuates amyloid deposition in middle-aged dtg APP/PS1 mice. Neuroscience letters. https://doi.org/10.1016/j.neulet.2009.08.038
Vancouver
Mouton PR, Chachich ME, Quigley C, Spangler E, Ingram DK. Caloric restriction attenuates amyloid deposition in middle-aged dtg APP/PS1 mice. Neuroscience letters. 2009. doi:10.1016/j.neulet.2009.08.038. PMID: 19699265.
BibTeX
@article{mouton2009-19699265,
author = {Mouton, P. R. and Chachich, M. E. and Quigley, C. and Spangler, E. and Ingram, D. K.},
title = {{Caloric restriction attenuates amyloid deposition in middle-aged dtg APP/PS1 mice}},
journal = {Neuroscience letters},
year = {2009},
doi = {10.1016/j.neulet.2009.08.038},
pmid = {19699265},
url = {https://doi.org/10.1016/j.neulet.2009.08.038}
}
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.
Key findings
- To evaluate the potential of CR to protect against relatively heavy AD-type pathology, middle-aged (13-14-month-old) mice that co-express two mutations related to familial AD, amyloid precursor protein (APP) and presenilin 1 (PS1), were fed balanced diets with 40% fewer calories than ad libitum-fed controls.
- Following 18 weeks of treatment, mice were killed and brains were processed for quantification of total volume of amyloid-beta (Abeta) in the hippocampal formation and the overlying neocortex.
- Computerized stereology confirmed that CR reduced the total Abeta volume by about one-third compared to that in age-matched controls.
- Thus, CR appears to attenuate the accumulation of AD-type neuropathology in two cortical brain regions of middle-aged dtg APP/PS1 mice.
Why it matters
Middle-aged mice carrying APP and PS1 mutations fed a diet with 40% fewer calories than controls showed reduced amyloid-beta volume in the hippocampal formation and overlying neocortex after 18 weeks. This is animal research only and does not show that caloric restriction prevents or treats Alzheimer disease in people.
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Study details
- Evidence strengthLow
How this study scored 42/100
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 (Neuroscience letters) |
| Journal's citation record | 3 / 4 | Neuroscience Letters: journal h-index 267 (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 | 2009 — 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 “app/ps1”) — scores zero |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 118 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 6.2 citations a year over 19 year(s) since 2009 |
| Impact for its field and year | 3 / 6 | Cited 3.7× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 1 / 4 | Cited 14 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Donald K. Ingram: h-index 88 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | National Institute on Aging: institution h-index 907 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 5 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 19699265) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 42 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1016/j.neulet.2009.08.038
- PubMed: 19699265
- 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).
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