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34/100

✓ Peer-reviewed alzhub usefulness score 34 out of 100. Tau biomarkers

Topic: Amyloid, tau and blood-test diagnosis

The BACE1 gene encodes the beta-site APP-cleaving enzyme 1 and has been associated with Alzheimer's disease (AD). BACE1 is the most important β-secretase responsible for the generation of Alzheimer-associated amyloid β-proteins (Aβ) and may play a role in the amyloidogenic process in AD. We hypothesized that BACE1 gene variants might influence BACE1 activity or other markers for APP metabolism in the cerebrospinal fluid (CSF) and thereby contribute to the development of AD.

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APA 7th

Sjölander, A., Zetterberg, H., Andreasson, U., Minthon, L., & Blennow, K. (2010). BACE1 gene variants do not influence BACE1 activity, levels of APP or Aβ isoforms in CSF in Alzheimer's disease. Molecular neurodegeneration. https://doi.org/10.1186/1750-1326-5-37

Vancouver

Sjölander A, Zetterberg H, Andreasson U, Minthon L, Blennow K. BACE1 gene variants do not influence BACE1 activity, levels of APP or Aβ isoforms in CSF in Alzheimer's disease. Molecular neurodegeneration. 2010. doi:10.1186/1750-1326-5-37. PMID: 20849576.

BibTeX

@article{sjolander2010-20849576,
  author  = {Sjölander, A. and Zetterberg, H. and Andreasson, U. and Minthon, L. and Blennow, K.},
  title   = {{BACE1 gene variants do not influence BACE1 activity, levels of APP or Aβ isoforms in CSF in Alzheimer's disease}},
  journal = {Molecular neurodegeneration},
  year    = {2010},
  doi     = {10.1186/1750-1326-5-37},
  pmid    = {20849576},
  url     = {https://doi.org/10.1186/1750-1326-5-37}
}

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Key findings

BACE1 is the most important β-secretase responsible for the generation of Alzheimer-associated amyloid β-proteins (Aβ) and may play a role in the amyloidogenic process in AD.
We hypothesized that BACE1 gene variants might influence BACE1 activity or other markers for APP metabolism in the cerebrospinal fluid (CSF) and thereby contribute to the development of AD.
We genotyped a Swedish sample of 269 AD patients for the rs638405 single nucleotide polymorphism (SNP) in the BACE1 gene and correlated genotype data to a broad range of amyloid-related biomarkers in CSF, including BACE1 activity, levels of Aβ40, Aβ42, α- and β-cleaved soluble APP (α-sAPP and β-sAPP), as well as markers for Alzheimer-type axonal degeneration, i.e., total-tau and phospho-tau181.
Gene variants of BACE1 were neither associated with amyloid-related biomarkers, nor with markers for axonal degeneration in AD.

Why it matters

This study found that BACE1 gene variants did not influence BACE1 activity, APP levels or amyloid beta isoforms in cerebrospinal fluid in Alzheimer's disease. It is a negative genetic finding about the amyloid pathway, not about treating, curing or preventing the disease.

New to this subject? Start with our plain-English guide: Blood tests & biomarkers →

Study details

Evidence strengthLow

How this study scored 34/100

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 (Molecular neurodegeneration)
Journal's citation record	2 / 4	Molecular Neurodegeneration: journal h-index 164 (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	2010 — 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	2 / 7	Cited 5 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.3 citations a year over 18 year(s) since 2010
Impact for its field and year	1 / 6	Cited 0.4× 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	0 / 4	Cited 1 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	4 / 4	Last-listed author Kaj Blennow: h-index 220 (OpenAlex, whole career)
Institution's track record	1 / 3	Lund University: institution h-index 1,119 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 3 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 20849576)
Free to read	2 / 2	Free to read
Total	34 / 100	—

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