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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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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79/100
✓ Peer-reviewed
alzhub usefulness score 79 out of 100.
·
JAMA
·
2026-07-13
The double-cutoff approach revealed high confidence for interpreting scans as negative when Centiloid values were lower than 11 (95% CI, 9-13; I2 = 95%) and interpreting scans as positive if Centiloid values were higher than 26 (95% CI, 24-28; I2 = 95%). 3 key findings →
Design: meta-analysis
Participants: 49,227
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.
·
PLoS medicine
·
2019-07-23
With no effective treatments for cognitive decline or dementia, improving the evidence base for modifiable risk factors is a research priority. 1 key finding →
Design: meta-analysis
Participants: 48,522
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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76/100
✓ Peer-reviewed
alzhub usefulness score 76 out of 100.
·
JAMA neurology
·
2020-11-01
Of 1583 articles, data subjected from the 24 studies (including 3562 patients who experienced delirium and 6987 controls who did not) were included in a random-effects meta-analysis for pooled effect estimates and random-effects meta-regressions to identify sources of study variance. 3 key findings →
Design: systematic review
Participants: 3,562
Evidence: high
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Adherence to a Mediterranean diet may contribute to the prevention of a series of brain diseases; this may be of special value given the aging of Western societies. 4 key findings →
Design: meta-analysis
Evidence: high
Full summary, score breakdown and related studies →
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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
Full summary, score breakdown and related studies →
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Midlife and late-life risk factors contributed to 22.7% and 16.5% of total dementia cases, respectively. 5 key findings →
Design: meta-analysis
Participants: 37,931
Evidence: high
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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
Full summary, score breakdown and related studies →
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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
·
2020-10-01
The largest cohort, the Anti-Amyloid Treatment in Asymptomatic Alzheimer Disease Study (n = 3154), was the PET screening cohort used for a secondary prevention trial designed to slow cognitive decline associated with brain amyloidosis. 3 key findings →
Design: meta-analysis
Participants: 3,154
Evidence: high
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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
Full summary, score breakdown and related studies →
Original source
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We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms. 2 key findings →
Design: meta-analysis
Participants: 17
Evidence: high
Full summary, score breakdown and related studies →
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TREM and TREM-like receptors are a structurally similar protein family encoded by genes clustered on chromosome 6p21.11. 4 key findings →
Design: meta-analysis
Evidence: high
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We identified a new genetic risk association of AD with rare coding CLU variations that is independent of the 5' common association signal identified in the GWA studies. 3 key findings →
Design: meta-analysis
Participants: 1,930
Evidence: high
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Two regions achieved genome-wide significance with TDP-43: apolipoprotein E (APOE) and TMEM106B. Three loci reached genome-wide significance with HS: APOE, TMEM106B, and granulin precursor (GRN). 5 key findings →
Design: meta-analysis
Participants: 9,509
Evidence: high
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Comprehensive and unbiased meta-analysis of all published and unpublished data from case-control studies for the SORL1 single-nucleotide polymorphisms (SNPs) that had been repeatedly assessed across studies. 4 key findings →
Design: meta-analysis
Participants: 12,464
Evidence: high
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65/100
✓ Peer-reviewed
alzhub usefulness score 65 out of 100.
·
PLoS Genetics
·
2025-03-17
The genetic component of early-onset Alzheimer disease (EOAD), accounting for ~10% of all Alzheimer's disease (AD) cases, is largely unexplained. 3 key findings →
Design: meta-analysis
Participants: 19,668
Evidence: high
Full summary, score breakdown and related studies →
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Much of the genetic basis for Alzheimer disease (AD) is unexplained. 4 key findings →
Design: meta-analysis
Evidence: high
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Forty-nine outcomes were presented to survey respondents. 4 key findings →
Design: systematic review
Evidence: high
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Amyloid beta (Aβ) peptides are the major components of senile plaques, one of the main pathological hallmarks of Alzheimer disease (AD). 4 key findings →
Design: meta-analysis
Evidence: high
Full summary, score breakdown and related studies →
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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.