Over a maximum follow-up of 26 years, the median time to event was 1·2 years (IQR 0·2-3·3) in the delirium group and 1·3 years (0·3-3·6) in the control group. 5 key findings →
Design: cohort study
Participants: 909
Evidence: moderate
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60/100
✓ Peer-reviewed
alzhub usefulness score 60 out of 100.
·
JAMA Network Open
·
2026-01-30
This study included 10 333 FHS 5 key findings →
Design: cohort study
Participants: 886
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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Hearing impairment is implicated as a risk factor for the incidence of all-cause dementia. 3 key findings →
Design: cohort study
Participants: 158,686
Evidence: moderate
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Original source
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57/100
✓ Peer-reviewed
alzhub usefulness score 57 out of 100.
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GeroScience
·
2026-05-22
Poor oral health and genetic susceptibility have each been linked to dementia risk, but their joint effects and subtype-specific associations remain unclear. 5 key findings →
Design: cohort study
Participants: 7,553
Evidence: moderate
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Shorter LTL was associated with an increased risk of NDDs, including Alzheimer's disease (HR: 0.52, 95% CI 0.40-0.67, P < 0.001), dementia in AD (HR: 0.53, 95% CI 0.39-0.73, P < 0.001), unspecified dementia (HR: 0.74, 95% CI 0.58-0.95, P < 0.05), degenerative diseases of the nervous system (including other specified degenerative diseases such as circumscribed brain atrophy and senile degeneration of the brain) (HR: 0.62, 95% CI 0.45-0.84, P < 0.01), extrapyramidal and movement disorders (including other specified extrapyramidal and movement disorders such as a range of tremors, chorea, tics, and other abnormal involuntary movements) (HR: 0.63, 95% CI 0.48-0.82, P < 0.01), and mental and behavioral disorders due to use of alcohol (HR: 0.46, 95% CI 0.38-0.55, P < 0.001). 5 key findings →
Participants: 459,902
Evidence: moderate
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Vestibular disorders were linked to higher risks of all‐cause dementia (HR 1.86 and 95% CI 1.04–3.30), Alzheimer's disease (AD, 2.36, and 1.01–5.51), and vascular dementia (VD, 3.35, and 1.48–7.59). 5 key findings →
Design: cohort study
Evidence: moderate
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During a median 13.7 years of follow-up, prediabetes (n=52,693) was associated with higher risks of vascular dementia (hazard ratio (HR):1.36; 95% confidence interval (CI): 1.14-1.61), stroke (HR:1.09; 95% CI: 1.01-1.16), ischemic stroke (HR:1.10; 95% CI: 1.02-1.19), and intracerebral hemorrhage (HR:1.19; 95% CI: 1.01-1.39) compared with normoglycemia, after adjustment for major confounding factors and across extensive sensitivity analyses. 5 key findings →
Participants: 52,693
Evidence: moderate
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Original source
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During a median 13.7 years of follow-up, prediabetes (n=52,693) was associated with higher risks of vascular dementia (hazard ratio (HR):1.36; 95% confidence interval (CI): 1.14-1.61), stroke (HR:1.09; 95% CI: 1.01-1.16), ischemic stroke (HR:1.10; 95% CI: 1.02-1.19), and intracerebral hemorrhage (HR:1.19; 95% CI: 1.01-1.39) compared with normoglycemia, after adjustment for major confounding factors and across extensive sensitivity analyses. 5 key findings →
Participants: 52,693
Evidence: moderate
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48/100
✓ Peer-reviewed
alzhub usefulness score 48 out of 100.
·
F1000Res
·
2026-07-22
This study contributes to the healthcare field by demonstrating the potential of providing a fast, transparent, and affordable assessment system that is accessible to low-income populations and clinics with limited budget. 2 key findings →
Evidence: moderate
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Original source
Inflammatory responses are characterized by the activation of immune cells, while inflammatory biomarkers intricately interact with the immune system. 4 key findings →
Design: cross-sectional
Evidence: moderate
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Three subtypes emerged: severe obesity-related inflammatory diabetes (SOID), mild metabolic diabetes (MMD, reference), and mild age-related hypertension-predominant diabetes (MARD-H). 5 key findings →
Evidence: low
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Accurate dementia risk prediction is challenging, and may be facilitated by better use of imaging and genetic data, including their complex interactions. 1 key finding →
Design: post-hoc analysis
Participants: 3,521
Evidence: low
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Participants were older adults (mean age 71.5 ± 8.7 years), primarily female (54.2%), and non-Hispanic White (96.5%). 5 key findings →
Evidence: low
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Our findings reinforce the notion of a bidirectional association between epilepsy and AD, providing proof-of-concept that epilepsy, especially late-onset, may be successfully integrated into AD risk frameworks. 5 key findings →
Evidence: moderate
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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
medRxiv (preprint)
·
2026-08-28
Impairment in the comprehension of morphosyntactic and transitivity information does not feature in current diagnostic guidelines for primary progressive aphasia (PPA) or Alzheimers Diseases (AD), despite research reporting delayed sensitivity or insensitivity of these clinical populations to these linguistic domains. 2 key findings →
Evidence: low
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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
medRxiv
·
2026-10-26
DNA cytosine modifications play a crucial role in gene regulation that underlies the pathogenesis of complex diseases such as Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies →
Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
medRxiv
·
2026-10-20
Longitudinal clinical cohorts contain heterogeneous progression patterns that are obscured by coarse diagnostic labels. 2 key findings →
Design: longitudinal study
Evidence: moderate
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Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
medRxiv
·
2026-10-09
Retirement timing alone showed limited association with later-life dementia risk, whereas sustained part-time employment and disability-related trajectories were more strongly associated with dementia risk. 5 key findings →
Participants: 13,879
Evidence: low
Full summary, score breakdown and related studies →
Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
Research Square
·
2026-10-06
The Alzheimer’s Disease Neuroimaging Initiative (ADNI) provides a comprehensive multimodal neuroimaging resource for studying aging and Alzheimer’s disease (AD). 5 key findings →
Design: longitudinal study
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
Research Square
·
2026-09-11
Brain aging reflects heterogeneous vascular-metabolic and neurodegenerative processes, yet brain age is often reduced to a gray matter (GM)-dominant estimate. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies →
Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
Research Square
·
2026-09-07
Alzheimer's disease classification by means of Magnetic Resonance Imaging demands strong models that are able to generalise to different stages of dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies →
Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
bioRxiv
·
2026-09-05
Sensitive human data underpin discoveries across medicine, biology and the social sciences, yet privacy regulation often prevents sharing them with collaborators or artificial intelligence (AI) systems. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
Research Square
·
2026-09-04
Risk prediction in Alzheimer disease can guide follow-up, biomarker testing, trial referral, and prognostic counseling. 1 key finding →
Participants: 1,002
Evidence: low
Full summary, score breakdown and related studies →
Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
bioRxiv
·
2026-09-03
The apolipoprotein E ε4 ( APOE ε4) allele is the strongest genetic risk factor for late-onset Alzheimer’s disease (AD), yet its associated protein changes across biofluids, brain regions, and cell types remain incompletely understood. 3 key findings →
Participants: 1,691
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
Research Square
·
2026-08-27
PTGDS followed a biphasic astrocytic trajectory with a statistically resolved donor-level inflection (quadratic term −2.27, p = 0.006; vertex at pseudo-progression score 0.47, bootstrap 95% confidence interval 0.32 to 0.53). 5 key findings →
Design: longitudinal study
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
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.