82/100
✓ Peer-reviewed
alzhub usefulness score 82 out of 100.
·
Nature genetics
·
2011-04-03
The Alzheimer Disease Genetics Consortium (ADGC) performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1) and two replication stages (stages 2 and 3). 1 key finding →
Design: meta-analysis
Evidence: high
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APOE ɛ4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. 5 key findings →
Design: meta-analysis
Participants: 4,203
Evidence: high
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78/100
✓ Peer-reviewed
alzhub usefulness score 78 out of 100.
·
JAMA
·
2013-04-01
Genome-wide significance in fully adjusted models (sex, age, APOE genotype, population stratification) was observed for a SNP in ABCA7 (rs115550680, allele = G; frequency, 0.09 cases and 0.06 controls; odds ratio [OR], 1.79 [95% CI, 1.47-2.12]; P = 2.2 × 10(-9)), which is in linkage disequilibrium with SNPs previously associated with Alzheimer disease in Europeans (0.8 Conclusions and relevance In this meta-analysis of data from African American participants, Alzheimer disease was significantly associated with variants in ABCA7 and with other genes that have been associated with Alzheimer disease in individuals of European ancestry. 4 key findings →
Design: meta-analysis
Participants: 5,896
Evidence: high
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78/100
✓ Peer-reviewed
alzhub usefulness score 78 out of 100.
·
JAMA neurology
·
2021-01-01
In addition, several loci associated with rare variants, including a genome-wide significant intergenic locus near IGF1R at 15q26 (P = 1.7 × 10-9) and 6 additional loci with suggestive significance (P ≤ 5 × 10-7) such as API5 at 11p12 (P = 8.8 × 10-8) and RBFOX1 at 16p13 (P = 5.4 × 10-7) were identified. 4 key findings →
Design: meta-analysis
Participants: 2,784
Evidence: high
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
·
JAMA
·
2023-02-21
In this exploratory analysis, the APOE ε3[R145C] missense variant was associated with an increased risk of AD among individuals of African ancestry with the ε3/ε4 genotype. 5 key findings →
Design: case-control
Participants: 31,929
Evidence: moderate
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The risk of developing Alzheimer's disease (AD) significantly increases in individuals carrying the APOEε4 allele. 5 key findings →
Design: case-control
Participants: 7,185
Evidence: moderate
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72/100
✓ Peer-reviewed
alzhub usefulness score 72 out of 100.
·
JAMA neurology
·
2014-11-01
Analysis confirmed the association of APOE with earlier AAO (P = 3.3 × 10(-96)), with associations in CR1 (rs6701713, P = 7.2 × 10(-4)), BIN1 (rs7561528, P = 4.8 × 10(-4)), and PICALM (rs561655, P = 2.2 × 10(-3)) reaching statistical significance (P Conclusions and relevance We confirmed an association of APOE (OMIM 107741) variants with AAO among affected participants with LOAD and observed novel associations of CR1 (OMIM 120620), BIN1 (OMIM 601248), and PICALM (OMIM 603025) with AAO. 3 key findings →
Design: meta-analysis
Participants: 9,162
Evidence: high
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64/100
✓ Peer-reviewed
alzhub usefulness score 64 out of 100.
·
JAMA neurology
·
2017-06-01
Protection from these ADP factors may be important for aging without significant ADP. 5 key findings →
Design: cohort study
Participants: 423
Evidence: moderate
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63/100
✓ Peer-reviewed
alzhub usefulness score 63 out of 100.
·
JAMA neurology
·
2026-04-01
Female individuals had higher plaque burden than male individuals (unadjusted odds ratio [OR], 1.97; 95% CI, 1.67-2.29; P Conclusions and relevance The findings indicate that female sex, APOEε4, and both race and African ancestry were jointly associated with amyloid in this study population. 3 key findings →
Design: cross-sectional
Participants: 2,268
Evidence: moderate
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62/100
✓ Peer-reviewed
alzhub usefulness score 62 out of 100.
·
Neurology
·
2012-06-20
CLU and MS4A4A eSNPs may at least partly explain the LOAD risk association at these loci. 3 key findings →
Evidence: low
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61/100
✓ Peer-reviewed
alzhub usefulness score 61 out of 100.
·
Neurology
·
2018-08-24
Our results indicate that APOE ε4 is independently associated with a greater severity of LB pathology. 5 key findings →
Design: case-control study
Evidence: moderate
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59/100
✓ Peer-reviewed
alzhub usefulness score 59 out of 100.
·
JAMA neurology
·
2018-11-01
The 751 study participants were older (median age [interquartile range], 87 years [51-105 years]), 395 (54%) were women, and 324 (44%) were APOE ε4 carriers. 5 key findings →
Design: cross-sectional
Participants: 604
Evidence: low
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Compared with individuals with the APOEepsilon3/epsilon3, the odds of having AD were significantly increased among those with 1 or more copies of the epsilon4 allele; the odds ratio (OR) for the epsilon3/epsilon4 genotype was 2.6 (95% confidence interval [CI], 1.8-3.7), and the OR for the epsilon4/epsilon4 genotype was 10.5 (95% CI, 5.1-21.8). 3 key findings →
Design: case-control study
Participants: 338
Evidence: moderate
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Apolipoprotein E (Apo-E) is a major cholesterol carrier that supports lipid transport and injury repair in the brain. 3 key findings →
Evidence: low
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Several heterozygous missense mutations in the triggering receptor expressed on myeloid cells 2 (TREM2) have recently been linked to risk for a number of neurological disorders including Alzheimer disease (AD), Parkinson disease, and frontotemporal dementia. 1 key finding →
Evidence: low
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These results suggest that GSTO locus variants may lower brain GSTO2 levels and consequently confer AD risk in older age. 5 key findings →
Evidence: low
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54/100
✓ Peer-reviewed
alzhub usefulness score 54 out of 100.
·
Neurology
·
2012-04-25
MLGPs provide an alternative analytical approach to predict an individual's genetic risk for episodic memory performance, a surrogate indicator of LOAD. 3 key findings →
Participants: 1,365
Evidence: low
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Polymorphism in the apolipoprotein E (APOE) gene is a major genetic risk determinant of late-onset Alzheimer disease (AD), with the APOE*ε4 allele conferring an increased risk and the APOE*ε2 allele conferring a decreased risk relative to the common APOE*ε3 allele. 2 key findings →
Evidence: low
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Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 3 key findings →
Evidence: low
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Apolipoprotein E (APOE) genotype is the major genetic risk factor for Alzheimer disease (AD); the ε4 allele increases risk and the ε2 allele is protective. 5 key findings →
Evidence: low
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Suspected non-Alzheimer disease pathophysiology (SNAP) is a biomarker-based concept that applies to individuals with normal levels of amyloid-β biomarkers in the brain, but in whom biomarkers of neurodegeneration are abnormal. 1 key finding →
Evidence: low
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Of 214 participants, 48 showed no decline on any test, 126 showed decline on only 1 test in 1 or more domains, and 40 showed decline on 2 or more tests in 1 or more domains. 2 key findings →
Participants: 214
Evidence: low
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APOE4 is the greatest risk factor for Alzheimer disease (AD) and synergistic effects with amyloid-β peptide (Aβ) suggest interactions among apoE isoforms and different forms of Aβ accumulation. 5 key findings →
Evidence: low
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Human apolipoprotein E (apoE) isoforms may differentially modulate amyloid-β (Aβ) levels. 5 key findings →
Evidence: moderate
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APOE2 is associated with less cognitive decline during aging. 5 key findings →
Evidence: low
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How the 0–100 score works — and why some entries are capped
This is alzhub's own score. It is not an official metric, not an impact factor,
and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a
scientist can tell a landmark trial from a conference abstract without having to already know the
difference. Every point comes from one of 20 components, all of them printed on the study itself,
so you can disagree with our arithmetic rather than having to trust the total.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
Journals are placed in ordered tiers, never given a numeric impact factor — we
could not verify current impact factors from a source we control, and an invented one would be
worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science,
Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed
journal. A separate part scores how much the journal's own papers are cited, which tells the
tier-3 journals apart.
Two rules we don't bend. First, we never fill in a
missing value: if a record does not state a sample size or a design, that component scores
zero, and if we simply have no data for a part, such as a citation count, that part is left out and
the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed
article is capped at 16/100 and carries a warning chip — so a conference abstract or
a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not
work — above an early positive finding. Someone deciding whether to buy a supplement is served by
that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is
reproducible: the same file always yields the same numbers.
See the whole rubric drawn out →
— four charts covering all 27,780 studies: how the scores are spread and where the cap
bites, which of the 20 components the library is strong and weak on, which subjects rest on
stronger evidence, and what kinds of study each subject is actually built from.