Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 57 out of 100. TREM2 and immune genetics

Topic: Amyloid, tau and blood-test diagnosis

Introduction The genetic risk effects of apolipoprotein E (APOE) on familial Alzheimer's disease (FAD) with or without gene mutations, sporadic AD (SAD), and normal controls (NC) remain unclear in the Chinese population. Methods In total, 15 119 subjects, including 311 FAD patients without PSEN1, PSEN2, APP, TREM2, and SORL1 pathogenic mutations (FAD [unknown]); 126 FAD patients with PSENs/APP mutations (FAD [PSENs/APP]); 7234 SAD patients; and 7448 NC were enrolled. The risk effects of APOE ε4 were analyzed across groups. Results The prevalence of the APOE ε4 genotype in FAD (unknown), FAD (PSENs/APP), SAD, and NC groups was 56.27%, 26.19%, 36.23%, and 19.54%, respectively. Further, the APOE ε4 positive genotype had predictive power for FAD (unknown) risk (odds ratio: 4.51, 95% confidence interval: 3.57-5.45, P < .001). Discussion APOE ε4 positive genotype may cause familial aggregation, and the investigation of multiple interventions targeting APOE pathological function to reduce the risk for this disease warrants attention.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Jia, L., Xu, H., Chen, S., Wang, X., Yang, J., Gong, M., et al. (2020). The APOE ε4 exerts differential effects on familial and other subtypes of Alzheimer's disease. Alzheimer's & dementia : the journal of the Alzheimer's Association. https://doi.org/10.1002/alz.12153

Vancouver

Jia L, Xu H, Chen S, Wang X, Yang J, Gong M, et al. The APOE ε4 exerts differential effects on familial and other subtypes of Alzheimer's disease. Alzheimer's & dementia : the journal of the Alzheimer's Association. 2020. doi:10.1002/alz.12153. PMID: 32881347.

BibTeX

@article{jia2020-32881347,
  author  = {Jia, L. and Xu, H. and Chen, S. and Wang, X. and Yang, J. and Gong, M. and Wei, C. and Tang, Y. and others},
  title   = {{The APOE ε4 exerts differential effects on familial and other subtypes of Alzheimer's disease}},
  journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
  year    = {2020},
  doi     = {10.1002/alz.12153},
  pmid    = {32881347},
  url     = {https://doi.org/10.1002/alz.12153}
}

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's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

Key findings

Study details

How this study scored 57/100
How this study's score is builtJournal tier 9 of 10; Journal's citation record left out, no data; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 2 of 5; Sample size 2 of 4; Effect reported 2 of 3; Studied in people 3 of 3; Randomised / blinded 0 of 2; Times cited left out, no data; Citations per year left out, no data; Impact for its field and year left out, no data; Cited by studies here left out, no data; Still being cited left out, no data; Senior author's track record left out, no data; Institution's track record left out, no data; Multi-centre collaboration left out, no data; Indexed in PubMed 2 of 2; Free to read 2 of 2. 33 of the 58 points it could be judged on, which is 57 of 100. Total 57 of 100.33 of the 58 points we could judge = 57 of 100

Published in a leading specialty journal. Scored zero for study design and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 33 of the 58 points we could judge it on, which is 57 out of 100.

ComponentPointsWhy
Journal tier 9 / 10 Tier 2 — leading specialty journal (Alzheimer's & dementia : the journal of the Alzheimer's Association)
Journal's citation record — / 4 No journal record from OpenAlex — left out of this score
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 2 / 5 2020 — within 10 year(s) of the newest study here
Sample size 2 / 4 119 participants
Effect reported 2 / 3 Effect reported as a number, without an interval or test
Studied in people 3 / 3 Studied in people (participant count stated)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited — / 7 No citation count (not found in OpenAlex) — left out of this score
Citations per year — / 5 No citation count or no year — left out of this score
Impact for its field and year — / 6 No field-weighted citation impact (OpenAlex has none yet) — left out of this score
Cited by studies here — / 6 Not yet checked against this library's citation graph — left out of this score
Still being cited — / 4 No yearly citation counts — left out of this score
Senior author's track record — / 4 Senior author's record not available — left out of this score
Institution's track record — / 3 No institution listed in OpenAlex — left out of this score
Multi-centre collaboration — / 3 Institutions not listed — left out of this score
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 32881347)
Free to read 2 / 2 Free to read
Points 33 / 58 Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 33 of the 58 points we could judge it on is 57 out of 100.
Total 57 / 100 —

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

Read the original

Free copy unknown: no free-copy check has an answer for this record yet. That does not mean it is paywalled.

Studies in the library that share something with this one. The line above each title says what.

Related studies in TREM2 and immune genetics

Also tagged “subtypes”

3 studies in the library carry the topic tag “subtypes”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 3 tagged studies.

Studies sharing this one's topic tags

Similar studies

More on TREM2 and immune genetics

See all studies in TREM2 and immune genetics →