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Aβ-degrading enzymes: potential for treatment of Alzheimer disease
Miners JS, Barua N, Kehoe PG, Gill S, Love S.. Journal of neuropathology and experimental neurology, 2011-11-01
Topic: Amyloid, tau and blood-test diagnosis
Plain-language summary
There is increasing evidence that deficient clearance of β-amyloid (Aβ) contributes to its accumulation in late-onset Alzheimer disease (AD). Several Aβ-degrading enzymes, including neprilysin (NEP), insulin-degrading enzyme, and endothelin-converting enzyme reduce Aβ levels and protect against cognitive impairment in mouse models of AD. The activity of several Aβ-degrading enzymes rises with age and increases still further in AD, perhaps as a physiological response to minimize the buildup of Aβ.
What this study adds
Evidence grade: Low
This is a narrative review. This paper reviews amyloid-beta-degrading enzymes that reduce amyloid-beta levels and protect against cognitive impairment in mouse models of Alzheimer's disease. The evidence comes from animal models, and the age- and disease-related changes in expression of some of these enzymes remain to be determined.
Taken from this record’s own fields, not from reading the paper. The grade is assigned from the abstract’s wording; what that means.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Miners, J. S., Barua, N., Kehoe, P. G., Gill, S., & Love, S. (2011). Aβ-degrading enzymes: potential for treatment of Alzheimer disease. Journal of neuropathology and experimental neurology. https://doi.org/10.1097/nen.0b013e3182345e46
Vancouver
Miners JS, Barua N, Kehoe PG, Gill S, Love S. Aβ-degrading enzymes: potential for treatment of Alzheimer disease. Journal of neuropathology and experimental neurology. 2011. doi:10.1097/nen.0b013e3182345e46. PMID: 22002425.
BibTeX
@article{miners2011-22002425,
author = {Miners, J. S. and Barua, N. and Kehoe, P. G. and Gill, S. and Love, S.},
title = {{Aβ-degrading enzymes: potential for treatment of Alzheimer disease}},
journal = {Journal of neuropathology and experimental neurology},
year = {2011},
doi = {10.1097/nen.0b013e3182345e46},
pmid = {22002425},
url = {https://doi.org/10.1097/nen.0b013e3182345e46}
}
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
- Several Aβ-degrading enzymes, including neprilysin (NEP), insulin-degrading enzyme, and endothelin-converting enzyme reduce Aβ levels and protect against cognitive impairment in mouse models of AD.
- The activity of several Aβ-degrading enzymes rises with age and increases still further in AD, perhaps as a physiological response to minimize the buildup of Aβ.
- The age- and disease-related changes in expression of more recently recognized Aβ-degrading enzymes (e.g.
- NEP-2 and cathepsin B) remain to be investigated, and there is strong evidence that reduced NEP activity contributes to the development of cerebral amyloid angiopathy.
Why it matters
This paper reviews amyloid-beta-degrading enzymes that reduce amyloid-beta levels and protect against cognitive impairment in mouse models of Alzheimer's disease. The evidence comes from animal models, and the age- and disease-related changes in expression of some of these enzymes remain to be determined.
Study details
- Evidence strengthLow
How this study scored 44/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology) |
| Journal's citation record | 2 / 4 | Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 | 2011 — 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 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 5 / 7 | Cited 265 times (OpenAlex, 2026-10-10) |
| Citations per year | 3 / 5 | 15.6 citations a year over 17 year(s) since 2011 |
| Impact for its field and year | 4 / 6 | Cited 14.9× 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 29 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author Seth Love: h-index 90 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | University of Bristol: institution h-index 1,260 (OpenAlex) |
| Multicenter collaboration | 1 / 3 | OpenAlex lists 2 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 22002425) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 44 / 100 | — |
What each of these 20 components measures, and what this score is not →
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