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
Full summary, score breakdown and related studies →
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In analyses that addressed bias due to reverse causation, physical inactivity was not associated with all-cause dementia or Alzheimer's disease, although an indication of excess dementia risk was observed in a subgroup of physically inactive individuals who developed cardiometabolic disease. 2 key findings →
Design: meta-analysis
Participants: 404
Evidence: high
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The first single-stage individual patient data meta-analysis from randomized double-blind placebo-controlled clinical trials provides evidence to support benefits of antihypertensive treatment in late-mid and later life to lower the risk of dementia. 5 key findings →
Design: meta-analysis
Participants: 28,008
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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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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79/100
✓ Peer-reviewed
alzhub usefulness score 79 out of 100.
·
JAMA neurology
·
2019-01-01
Of 2846 articles identified, 94 studies were eligible, with up to 14 529 participants for WMH, 16 012 participants for BI, 15 693 participants for CMB, and 4587 participants for PVS. 2 key findings →
Design: meta-analysis
Participants: 529
Evidence: high
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The task force issued five statements related to the management of anxiety, agitation/sedation, delirium, immobility, and sleep disruption in adults admitted to the ICU. 5 key findings →
Design: systematic review
Participants: 24
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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Ann Neurol 2018;84:737-748. 1 key finding →
Design: meta-analysis
Participants: 443
Evidence: high
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Dementia has been increasingly more recognized to be a common feature in patients with Parkinson's disease (PD), especially in old age. 4 key findings →
Design: systematic review
Evidence: high
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This large GWAS of WMH burden in community-based cohorts of individuals of European descent identifies a novel locus on chromosome 17. 5 key findings →
Design: meta-analysis
Participants: 3,024
Evidence: high
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Over a long period of observation, no evidence was found that a specific AHM drug class was more effective than others in lowering risk of dementia. 4 key findings →
Design: meta-analysis
Participants: 31
Evidence: high
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73/100
✓ Peer-reviewed
alzhub usefulness score 73 out of 100.
·
Neurology
·
2022-11-14
We included randomized controlled trials (RCTs) and nonrandomized controlled studies at lower risk of bias comparing ChEI treatment with placebo or usual treatment, for 6 months or longer, in patients with dementia of any type. 5 key findings →
Design: systematic review
Participants: 79,153
Evidence: high
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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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Genome-wide association studies (GWAS) have identified a region upstream the BIN1 gene as the most important genetic susceptibility locus in Alzheimer's disease (AD) after APOE. 1 key finding →
Design: meta-analysis
Evidence: high
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Neuroinflammation commences decades before Alzheimer's disease (AD) clinical onset and represents one of the earliest pathomechanistic alterations throughout the AD continuum. 4 key findings →
Design: meta-analysis
Evidence: high
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Being married is associated with reduced risk of dementia than widowed and lifelong single people, who are also underdiagnosed in routine clinical practice. 5 key findings →
Design: systematic review
Participants: 15
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
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71/100
✓ Peer-reviewed
alzhub usefulness score 71 out of 100.
·
Stroke
·
2020-06-10
Periventricular white matter hyperintensities (WMH; PVWMH) and deep WMH (DWMH) are regional classifications of WMH and reflect proposed differences in cause. 4 key findings →
Design: meta-analysis
Participants: 26,654
Evidence: high
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We performed a systematic review of studies focusing on the automatic prediction of the progression of mild cognitive impairment to Alzheimer's disease (AD) dementia, and a quantitative analysis of the methodological choices impacting performance. 1 key finding →
Design: systematic review
Participants: 172
Evidence: high
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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
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Whether novel risk variants of Alzheimer's disease (AD) identified through genome-wide association studies also influence magnetic resonance imaging-based intermediate phenotypes of AD in the general population is unclear. 4 key findings →
Design: meta-analysis
Participants: 8,175
Evidence: high
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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.