General cognitive function is substantially heritable across the human life course from adolescence to old age. 5 key findings →
Design: meta-analysis
Participants: 53,949
Evidence: high
Full summary, score breakdown and related studies →
Original source
84/100
✓ Peer-reviewed
alzhub usefulness score 84 out of 100.
·
JAMA
·
2015-05-01
Among persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. 4 key findings →
Design: meta-analysis
Participants: 2,914
Evidence: high
Full summary, score breakdown and related studies →
Original source
Free full text
We identified four plasma protein level PGSs that were significantly associated (FDR-adjusted p < 0.05) with LOAD in a meta-analysis of the discovery and replication cohorts: CX3CL1, hepatocyte growth factor (HGF), TIE2, and matrix metalloproteinase-3 (MMP-3). 4 key findings →
Design: meta-analysis
Participants: 17,747
Evidence: high
Full summary, score breakdown and related studies →
Original source
Mass spectrometry-based proteomics empowers deep profiling of proteome and protein posttranslational modifications (PTMs) in Alzheimer's disease (AD). 5 key findings →
Design: meta-analysis
Participants: 12,017
Evidence: high
Full summary, score breakdown and related studies →
Original source
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
Full summary, score breakdown and related studies →
Original source
Free full text
Alzheimer's disease (AD) is the most common multifactorial neurodegenerative disease among elderly people. 2 key findings →
Design: meta-analysis
Participants: 140
Evidence: high
Full summary, score breakdown and related studies →
Original source
Autopsy measures of Alzheimer's disease neuropathology have been leveraged as endophenotypes in previous genome-wide association studies (GWAS). 2 key findings →
Design: meta-analysis
Participants: 2,701
Evidence: high
Full summary, score breakdown and related studies →
Original source
We identified and validated five novel gene associations in cortical brain tissue ( PRKAG1 , C3orf62 , LYSMD4 , ZNF439 , SLC11A2 ) and six genes proximal to known AD-related GWAS loci (Blood: MYBPC3 ; Brain: MTCH2 , CYB561 , MADD , PSMA5 , ANXA11 ). 3 key findings →
Design: meta-analysis
Participants: 2,683
Evidence: high
Full summary, score breakdown and related studies →
Original source
81/100
✓ Peer-reviewed
alzhub usefulness score 81 out of 100.
·
Nature Genetics
·
2026-06-23
This 2026 update is an even larger follow-up to the 2022 Bellenguez GWAS, combining data from nearly 1 million people. 5 key findings →
Design: meta-analysis
Participants: 978,514
Evidence: high
Full summary, score breakdown and related studies →
Original source
81/100
✓ Peer-reviewed
alzhub usefulness score 81 out of 100.
·
Nature genetics
·
2018-06-25
Intelligence is highly heritable 1 and a major determinant of human health and well-being 2 . 2 key findings →
Design: meta-analysis
Participants: 269,867
Evidence: high
Full summary, score breakdown and related studies →
Original source
81/100
✓ Peer-reviewed
alzhub usefulness score 81 out of 100.
·
Nature genetics
·
2017-01-16
Collecting cases for case-control genetic association studies can be time-consuming and expensive. 1 key finding →
Design: meta-analysis
Participants: 116,196
Evidence: high
Full summary, score breakdown and related studies →
Original source
Due to the small number of studies and heterogeneity in study design and outcomes, the association between DNA methylation age and age-related disease and longevity is inconclusive. 3 key findings →
Design: systematic review
Participants: 41,607
Evidence: high
Full summary, score breakdown and related studies →
Original source
Iron deposition in the brain is a prominent feature of Alzheimer's disease (AD). 3 key findings →
Design: meta-analysis
Participants: 24,000
Evidence: high
Full summary, score breakdown and related studies →
Original source
Alzheimer's disease (AD) is the most common neurodegenerative disease. 2 key findings →
Design: meta-analysis
Participants: 74,046
Evidence: high
Full summary, score breakdown and related studies →
Original source
The objective of this meta-analysis was to determine the association of the apolipoprotein E ( ApoE ) gene with exceptional longevity (EL) ( i.e ., reaching 100+ years) by identifying possible unequal distribution of alleles/genotypes in the common variants ε2, ε3, and ε4 among centenarians and younger population. 4 key findings →
Design: meta-analysis
Participants: 2,776
Evidence: high
Full summary, score breakdown and related studies →
Original source
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
Full summary, score breakdown and related studies →
Original source
Free full text
These results provide new insight into the genetic basis of habitual PA, and the genetic links connecting PA with other traits and diseases. 5 key findings →
Design: meta-analysis
Participants: 8,556
Evidence: high
Full summary, score breakdown and related studies →
Original source
In the replication stage, we performed genotyping of significant and suggestive results from the discovery stage. 2 key findings →
Design: meta-analysis
Participants: 1,743
Evidence: high
Full summary, score breakdown and related studies →
Original source
Narcolepsy type 1 is strongly associated with human leukocyte antigen (HLA)-DQB1*06:02; however, no significant associations between IH and HLA alleles have been reported. 4 key findings →
Design: meta-analysis
Participants: 414
Evidence: high
Full summary, score breakdown and related studies →
Original source
The aims of this study were to identify candidate single nucleotide polymorphisms (SNPs) and mechanisms of Alzheimer's disease (AD) and to generate SNP to gene to pathway hypotheses. 5 key findings →
Design: meta-analysis
Participants: 370,542
Evidence: high
Full summary, score breakdown and related studies →
Original source
GWAS of Alzheimer's disease have been predominantly based on European ancestry cohorts with clinically diagnosed patients. 2 key findings →
Design: meta-analysis
Evidence: high
Full summary, score breakdown and related studies →
Original source
Identifying ancestry-specific molecular profiles of late-onset Alzheimer's Disease (LOAD) in brain tissue is crucial to understand novel mechanisms and develop effective interventions in non-European, high-risk populations. 3 key findings →
Design: meta-analysis
Participants: 731
Evidence: high
Full summary, score breakdown and related studies →
Original source
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
Full summary, score breakdown and related studies →
Original source
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
Full summary, score breakdown and related studies →
Original source
Free full text
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
Full summary, score breakdown and related studies →
Original source
Free full text
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.