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44/100

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Risk genes beyond APOE

Topic: Brain proteins, microglia and lab models

The aspartyl protease beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) initiates processing of amyloid precursor protein (APP) into amyloid beta (Abeta) peptide, the major component of Alzheimer disease (AD) plaques. To determine the role that BACE1 plays in the development of Abeta-driven AD-like pathology, we have crossed PDAPP mice, a transgenic mouse model of AD overexpressing human mutated APP, onto mice with either a homozygous or heterozygous BACE1 gene knockout. Analysis of PDAPP/BACE(-/-) mice demonstrated that BACE1 is absolutely required for both Abeta generation and the development of age-associated plaque pathology.

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APA 7th

McConlogue, L., Buttini, M., Anderson, J. P., Brigham, E. F., Chen, K. S., Freedman, S. B., et al. (2007). Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice. The Journal of biological chemistry. https://doi.org/10.1074/jbc.m611687200

Vancouver

McConlogue L, Buttini M, Anderson JP, Brigham EF, Chen KS, Freedman SB, et al. Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice. The Journal of biological chemistry. 2007. doi:10.1074/jbc.m611687200. PMID: 17616527.

BibTeX

@article{mcconlogue2007-17616527,
  author  = {McConlogue, L. and Buttini, M. and Anderson, J. P. and Brigham, E. F. and Chen, K. S. and Freedman, S. B. and Games, D. and Johnson-Wood, K. and others},
  title   = {{Partial reduction of BACE1 has dramatic effects on Alzheimer plaque and synaptic pathology in APP Transgenic Mice}},
  journal = {The Journal of biological chemistry},
  year    = {2007},
  doi     = {10.1074/jbc.m611687200},
  pmid    = {17616527},
  url     = {https://doi.org/10.1074/jbc.m611687200}
}

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Key findings

To determine the role that BACE1 plays in the development of Abeta-driven AD-like pathology, we have crossed PDAPP mice, a transgenic mouse model of AD overexpressing human mutated APP, onto mice with either a homozygous or heterozygous BACE1 gene knockout.
Analysis of PDAPP/BACE(-/-) mice demonstrated that BACE1 is absolutely required for both Abeta generation and the development of age-associated plaque pathology.
Furthermore, synaptic deficits, a neurodegenerative pathology characteristic of AD, were also reversed in the bigenic mice.
To determine the extent of BACE1 reduction required to significantly inhibit pathology, PDAPP mice having a heterozygous BACE1 gene knock-out were evaluated for Abeta generation and for the development of pathology.

Why it matters

In a mouse model of Alzheimer's disease, removing the BACE1 gene prevented amyloid-beta generation and plaque pathology, and partially reducing BACE1 also reduced synaptic deficits. This is animal research, so it supports BACE1 as a possible target but does not prove that lowering BACE1 helps people.

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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 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 biological chemistry)
Journal's citation record	4 / 4	Journal of Biological Chemistry: journal h-index 780 (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	2007 — 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 “transgenic”) — 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 299 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	14.2 citations a year over 21 year(s) since 2007
Impact for its field and year	4 / 6	Cited 12.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	3 / 6	Cited by 18 other studies in this library
Still being cited	2 / 4	Cited 16 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Sukanto Sinha: h-index 31 (OpenAlex, whole career)
Institution's track record	0 / 3	Elan Pharmaceuticals, Inc. (Ireland): institution h-index 241 (OpenAlex)
Multi-centre collaboration	0 / 3	OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 17616527)
Free to read	0 / 2	Behind a paywall — scores zero
Total	44 / 100	—

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