85/100
✓ Peer-reviewed
alzhub usefulness score 85 out of 100.
·
Nature genetics
·
2019-02-28
Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics. 5 key findings →
Design: meta-analysis
Participants: 94,437
Evidence: high
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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
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82/100
✓ Peer-reviewed
alzhub usefulness score 82 out of 100.
·
JAMA
·
2015-05-01
The likelihood of amyloid positivity was associated with age and APOE ε4 status. 3 key findings →
Design: meta-analysis
Participants: 377
Evidence: high
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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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82/100
✓ Peer-reviewed
alzhub usefulness score 82 out of 100.
·
Nature genetics
·
2017-07-17
We identified rare coding variants associated with Alzheimer's disease in a three-stage case-control study of 85,133 subjects. 4 key findings →
Design: case-control study
Participants: 85,133
Evidence: moderate
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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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Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. 4 key findings →
Design: meta-analysis
Participants: 3,526
Evidence: high
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77/100
✓ Peer-reviewed
alzhub usefulness score 77 out of 100.
·
Genome biology
·
2025-07-17
Using cross-population GWAS meta-analyses, we identify novel LOAD susceptibility loci in/near LRRC4C and LHX5-AS1, both with known roles in neuronal development, as well as several novel population-unique loci. 1 key finding →
Design: meta-analysis
Participants: 409,589
Evidence: high
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Ann Neurol 2018;84:737-748. 1 key finding →
Design: meta-analysis
Participants: 443
Evidence: high
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76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
·
JAMA network open
·
2025-03-03
Age, sex, and apolipoprotein E (APOE) are the strongest risk factors for late-onset Alzheimer disease (AD). 4 key findings →
Design: meta-analysis
Participants: 4,592
Evidence: high
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A rare variant in TREM2 (p.R47H, rs75932628) was recently reported to increase the risk of Alzheimer's disease (AD) and, subsequently, other neurodegenerative diseases, i.e. frontotemporal lobar degeneration (FTLD), amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD). 4 key findings →
Design: meta-analysis
Participants: 828
Evidence: high
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Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) is a fatal neurodegenerative disorder with only a limited number of risk loci identified. 3 key findings →
Design: meta-analysis
Participants: 985
Evidence: high
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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
·
2021-04-07
We tested the hypothesis that plasma neurofilament light chain (NfL) identifies asymptomatic carriers of familial frontotemporal lobar degeneration (FTLD)-causing mutations at risk of disease progression. 4 key findings →
Design: longitudinal study
Participants: 277
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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Hippocampal sclerosis of aging (HS-Aging) is a high-morbidity brain disease in the elderly but risk factors are largely unknown. 4 key findings →
Design: meta-analysis
Participants: 624
Evidence: high
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71/100
✓ Peer-reviewed
alzhub usefulness score 71 out of 100.
·
JAMA neurology
·
2018-08-01
After correcting for multiple comparisons using the Bonferroni procedure, we observed a statistically significant interaction between APOE-ε4 and sex on CSF total tau (β = 0.41; 95% CI, 0.27-0.55; P Conclusions and relevance We provide robust evidence of a stronger association between APOE-ε4 and CSF tau levels among women compared with men across multiple independent data sets. 5 key findings →
Design: cohort study
Participants: 1,798
Evidence: moderate
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71/100
✓ Peer-reviewed
alzhub usefulness score 71 out of 100.
·
JAMA neurology
·
2013-06-01
We found a significant association between GBA1 mutation carrier status and DLB, with an odds ratio of 8.28 (95% CI, 4.78-14.88). 3 key findings →
Design: meta-analysis
Evidence: high
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71/100
✓ Peer-reviewed
alzhub usefulness score 71 out of 100.
·
Nature medicine
·
2024-05-14
GRN mutations cause progranulin haploinsufficiency, which eventually leads to frontotemporal dementia (FTD-GRN). 4 key findings →
Design: clinical trial
Evidence: moderate
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71/100
✓ Peer-reviewed
alzhub usefulness score 71 out of 100.
·
PLoS medicine
·
2018-01-09
We found up to 270-fold genetic enrichment between FTD and RA, up to 160-fold genetic enrichment between FTD and UC, up to 180-fold genetic enrichment between FTD and T1D, and up to 175-fold genetic enrichment between FTD and CeD. 5 key findings →
Design: meta-analysis
Participants: 192,886
Evidence: low
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White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. 1 key finding →
Evidence: moderate
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69/100
✓ Peer-reviewed
alzhub usefulness score 69 out of 100.
·
JAMA neurology
·
2013-02-01
The APOE ϵ4 allele is a strong risk factor across the LBD spectrum and occurs at an increased frequency in pDLB relative to PDD. 4 key findings →
Design: case-control study
Participants: 244
Evidence: moderate
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69/100
✓ Peer-reviewed
alzhub usefulness score 69 out of 100.
·
PloS one
·
2013-04-02
To discover susceptibility genes of late-onset Alzheimer's disease (LOAD), we conducted a 3-stage genome-wide association study (GWAS) using three populations: Japanese from the Japanese Genetic Consortium for Alzheimer Disease (JGSCAD), Koreans, and Caucasians from the Alzheimer Disease Genetic Consortium (ADGC). 1 key finding →
Participants: 1,008
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 27,380 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.