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46/100

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Risk genes beyond APOE

Topic: Brain proteins, microglia and lab models

Plain-language summary

Amyloid β (Aβ) damages neurons and triggers microglial inflammatory activation in the Alzheimer disease (AD) brain. BACE1 is the primary enzyme in Aβ generation. Neuroinflammation potentially up-regulates BACE1 expression and increases Aβ production.

What this study adds

Evidence grade: Low

In transgenic mice and SH-SY5Y cells, reducing p38alpha MAPK facilitated lysosomal degradation of BACE1 and attenuated amyloid pathology. This is animal and cell-model evidence and does not demonstrate that targeting p38alpha MAPK treats or prevents Alzheimer's disease in people.

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

Schnöder, L., Hao, W., Qin, Y., Liu, S., Tomic, I., Liu, X., et al. (2016). Deficiency of Neuronal p38α MAPK Attenuates Amyloid Pathology in Alzheimer Disease Mouse and Cell Models through Facilitating Lysosomal Degradation of BACE1. The Journal of biological chemistry. https://doi.org/10.1074/jbc.m115.695916

Vancouver

Schnöder L, Hao W, Qin Y, Liu S, Tomic I, Liu X, et al. Deficiency of Neuronal p38α MAPK Attenuates Amyloid Pathology in Alzheimer Disease Mouse and Cell Models through Facilitating Lysosomal Degradation of BACE1. The Journal of biological chemistry. 2016. doi:10.1074/jbc.m115.695916. PMID: 26663083.

BibTeX

@article{schnoder2016-26663083,
  author  = {Schnöder, L. and Hao, W. and Qin, Y. and Liu, S. and Tomic, I. and Liu, X. and Fassbender, K. and Liu, Y.},
  title   = {{Deficiency of Neuronal p38α MAPK Attenuates Amyloid Pathology in Alzheimer Disease Mouse and Cell Models through Facilitating Lysosomal Degradation of BACE1}},
  journal = {The Journal of biological chemistry},
  year    = {2016},
  doi     = {10.1074/jbc.m115.695916},
  pmid    = {26663083},
  url     = {https://doi.org/10.1074/jbc.m115.695916}
}

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 names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.

How to read this study

Design: our record does not state a study design, so check the methods section of the original before weighing the result.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

New to reading papers? Six questions to ask of any Alzheimer’s study · how we score.

Key findings

BACE1 is the primary enzyme in Aβ generation.
Neuroinflammation potentially up-regulates BACE1 expression and increases Aβ production.
In Alzheimer amyloid precursor protein-transgenic mice and SH-SY5Y cell models, we specifically knocked out or knocked down gene expression of mapk14, which encodes p38α MAPK, a kinase sensitive to inflammatory and oxidative stimuli.
Using immunological and biochemical methods, we observed that reduction of p38α MAPK expression facilitated the lysosomal degradation of BACE1, decreased BACE1 protein and activity, and subsequently attenuated Aβ generation in the AD mouse brain.

Why it matters

New to this subject? Start with our plain-English guide: Genetics →

Study details

Evidence strengthLow

How this study scored 46/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / 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	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
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	5 / 7	Cited 148 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	12.3 citations a year over 12 year(s) since 2016
Impact for its field and year	3 / 6	Cited 7.1× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	1 / 6	Cited by 1 other studies in this library
Still being cited	2 / 4	Cited 40 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Yang Liu: h-index 50 (OpenAlex, whole career)
Institution's track record	3 / 3	Harvard University: institution h-index 3,235 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 3 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 26663083)
Free to read	0 / 2	Behind a paywall — scores zero
Total	46 / 100	—

What each of these 20 components measures, and what this score is not →

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