The need for large sample sizes has led to collaborative efforts, such as the Prospective Studies Collaboration (an individual participant meta-analysis of data from 61 studies and more than a million participants11) that has demonstrated conclusively that a continuous increase in blood pressure corresponds with an increased risk of vascular death across all age groups (see Figure 1 that illustrates the importance of a large sample size (about 500 000 participants) for detecting this association).12 Sample size is also of particular importance in the current era of genome-wide association studies, where many investigations are aiming to detect either small effects from common variants or large effects from rare variants.13 Absolute risk of ischaemic heart disease mortality by usual systolic blood pressure and age at risk in 5000, 50 000, and 500 000 participants. 5 key findings →
Design: meta-analysis
Participants: 5,200
Evidence: high
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78/100
✓ Peer-reviewed
alzhub usefulness score 78 out of 100.
·
JAMA
·
2010-05-01
Two loci were identified to have genome-wide significance for the first time: rs744373 near BIN1 (odds ratio [OR],1.13; 95% confidence interval [CI],1.06-1.21 per copy of the minor allele; P = 1.59x10(-11)) and rs597668 near EXOC3L2/BLOC1S3/MARK4 (OR, 1.18; 95% CI, 1.07-1.29; P = 6.45x10(-9)). 3 key findings →
Participants: 35,000
Evidence: low
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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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77/100
✓ Peer-reviewed
alzhub usefulness score 77 out of 100.
·
Nature Genetics
·
2022-04
This was, at the time, the largest genetic study of Alzheimer's disease ever done, comparing DNA from over 111,000 people with the disease (or a strong family history) to nearly 680,000 people without it. 4 key findings →
Design: meta-analysis
Participants: 788,989
Evidence: high
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76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
·
Nature genetics
·
2007-01-01
The past decade has witnessed hundreds of reports declaring or refuting genetic association with putative Alzheimer disease susceptibility genes. 1 key finding →
Design: meta-analysis
Evidence: high
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Ann Neurol 2018;84:737-748. 1 key finding →
Design: meta-analysis
Participants: 443
Evidence: high
Full summary, score breakdown and related studies →
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This situation presents difficulties for experimental studies, drug development, and other future research. 5 key findings →
Design: meta-analysis
Participants: 94
Evidence: high
Full summary, score breakdown and related studies →
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75/100
✓ Peer-reviewed
alzhub usefulness score 75 out of 100.
·
Neurology
·
2014-06-13
Significant proportions of the observed variance in age at symptom onset in ADAD can be explained by family history and mutation type, providing empirical support for use of these data to estimate onset in clinical research. 2 key findings →
Participants: 3,275
Evidence: low
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Lewy body dementia (LBD) is the second most prevalent dementia, however most genetic risk remains uncharacterized. 5 key findings →
Design: meta-analysis
Evidence: high
Full summary, score breakdown and related studies →
Original source
APOE4 confers greater AD risk in women. 5 key findings →
Design: case-control study
Participants: 5,496
Evidence: moderate
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74/100
✓ Peer-reviewed
alzhub usefulness score 74 out of 100.
·
JAMA neurology
·
2017-10-01
Contrary to long-standing views, men and women with the APOE ε3/ε4 genotype have nearly the same odds of developing AD from age 55 to 85 years, but women have an increased risk at younger ages. 5 key findings →
Design: case-control study
Evidence: moderate
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74/100
✓ Peer-reviewed
alzhub usefulness score 74 out of 100.
·
Neurology
·
2020-02-11
We identified 2 core dimensions of heterogeneity: typicality and severity. 2 key findings →
Design: systematic review
Evidence: high
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Avagacestat dosed at 25 and 50 mg daily was relatively well tolerated and had low discontinuation rates. 2 key findings →
Design: clinical trial
Participants: 209
Evidence: high
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The APOE ε4 allele remains the strongest genetic risk factor for sporadic Alzheimer's disease and the APOE ε2 allele the strongest genetic protective factor after multiple large scale genome-wide association studies and genome-wide association meta-analyses. 5 key findings →
Design: meta-analysis
Evidence: high
Full summary, score breakdown and related studies →
Original source
74/100
✓ Peer-reviewed
alzhub usefulness score 74 out of 100.
·
Nature genetics
·
2021-02-15
Genome-wide association studies have discovered numerous genomic loci associated with Alzheimer's disease (AD); yet the causal genes and variants are incompletely identified. 2 key findings →
Design: meta-analysis
Evidence: high
Full summary, score breakdown and related studies →
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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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Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074
Evidence: low
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
·
Neurology
·
2008-01-01
In moderate stages of amnestic mild cognitive impairment, common cognitive tests provide better predictive accuracy than measures of whole brain, ventricular, entorhinal cortex, or hippocampal volumes for assessing progression to Alzheimer disease. 1 key finding →
Participants: 129
Evidence: high
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
·
Genes
·
2020-12-22
The primary genetic risk factor for late onset Alzheimer's disease (LOAD) is the APOE4 allele of Apolipoprotein E (APOE) gene. 2 key findings →
Design: meta-analysis
Evidence: high
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
·
Biomedicines
·
2024-06-22
Cognitive impairment was observed in 65 patients (42.5%) during a mean follow-up of 37.7 ± 12.4 months. 5 key findings →
Design: cohort study
Participants: 153
Evidence: moderate
Full summary, score breakdown and related studies →
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Genome-wide association studies (GWAS) of Alzheimer's disease are predominantly carried out in European ancestry individuals despite the known variation in genetic architecture and disease prevalence across global populations. 1 key finding →
Design: meta-analysis
Evidence: high
Full summary, score breakdown and related studies →
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Clinical data supported a delayed onset of cognitive impairment in persons who were heterozygous for the APOE3 Ch variant in a kindred with a high prevalence of autosomal dominant Alzheimer's disease. 3 key findings →
Design: cohort
Participants: 1,077
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.
·
Neurology
·
2010-06-30
Patients with MCI converted to AD at an annual rate of 17.2%. 2 key findings →
Design: longitudinal study
Participants: 85
Evidence: moderate
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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 27,380 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.