Our sample included 1001 participating and 3873 matched control SNFs. 5 key findings →
Design: cohort study Participants: 1,001 Evidence: moderate
Full summary, score breakdown and related studies → Original source
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Our sample included 1001 participating and 3873 matched control SNFs. 5 key findings →
Design: cohort study Participants: 1,001 Evidence: moderate
Full summary, score breakdown and related studies → Original source
From the 868 Framingham Heart Study participants who returned for a second PSG, this cohort included 346 participants with a mean age of 69 years (range, 60-87 years); 179 (52%) were female. 4 key findings →
Design: cohort Participants: 346 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline. 5 key findings →
Design: cohort Participants: 2,684 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Of 23 558 people without pre-existing dementia, 4135 (17·6%) had an admission with delirium. 5 key findings →
Design: cohort Participants: 23,558 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Frailty, comorbidities, and other age-related diseases were associated with a higher risk of dementia but did not account for the elevated dementia risk observed after severe infections. 3 key findings →
Design: cohort Participants: 449,223 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid NFL concentration (median [interquartile range]) was higher in the AD dementia group (1479 [1134-1842] pg/mL), stable MCI group (no progression to AD during follow-up; 1182 [923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during follow-up; 1336 [1061-1693] pg/mL) compared with control participants (1047 [809-1265] pg/mL) (P Conclusions and relevance Cerebrospinal fluid NFL concentration is increased by the early clinical stage of AD and is associated with cognitive deterioration and structural brain changes over time. 2 key findings →
Design: longitudinal study Participants: 95 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neurofilament proteins have been validated as specific body fluid biomarkers of neuro-axonal injury. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 641 participants with CSF Aβ42 data and at least two 18F-florbetapir scans, 335 (52.3%) were male. 4 key findings →
Design: cohort study Participants: 402 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Both high baseline GFAP (hazard ratio 3·6, 95% CI 2·2-5·7; p 42/40 , both GFAP (2·6, 1·4-5·0; p=0·0026) and amyloid β 42/40 (2·1, 1·2-3·6; p=0·0091) were independently associated with incident dementia whereas NfL was not (1·4, 0·8-2·5; p=0·28). 2 key findings →
Design: cohort study Participants: 300 Evidence: moderate
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Our findings show that different AT(N) variants are not interchangeable, and that optimal variants differ by clinical stage. 4 key findings →
Design: longitudinal study Participants: 490 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Most neuroinflammatory CSF biomarkers were associated with WML in individuals without dementia. 5 key findings →
Design: longitudinal study Participants: 247 Evidence: moderate
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Among community-dwelling adults included in this study, higher fragmentation of the 24-hour activity rhythms was associated with greater subsequent Aβ burden, especially in APOE4 carriers. 5 key findings →
Design: cohort study Participants: 639 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →
Design: cohort study Participants: 137 Evidence: moderate
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These results from the largest longitudinal cohort registry of patients with CAA-ri support the transient and potentially relapsing inflammatory nature of the clinical-radiologic acute manifestations of the disease and the effectiveness of slow oral tapering off after IV corticosteroid pulse therapy in preventing recurrences. 3 key findings →
Design: longitudinal study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In subjects with MCI and evidence of amyloid pathology, the injury markers CSF t-tau and p-tau and hippocampal atrophy can predict further cognitive decline. 1 key finding →
Design: cohort study Participants: 110 Evidence: moderate
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Fasting lipid fractions (triglycerides [TGs], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC]) were studied as continuous variables, and results are reported per SD increase of each lipid fraction. 5 key findings →
Design: cohort study Participants: 9,294 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Diabetes prevention and glucose control in midlife may protect against late-life cognitive decline. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A combination of modifiable vascular risk factors in midlife is highly predictive of the likelihood of dementia decades later. 1 key finding →
Design: cohort study Participants: 2,767 Evidence: moderate
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Atrial fibrillation, hypertension, and angina were associated with a greater rate of decline and may represent modifiable risk factors for secondary prevention in Alzheimer disease. 3 key findings →
Design: longitudinal study Participants: 135 Evidence: moderate
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Our results suggest that having an increased body weight or abdominal obesity are associated with increased dementia incidence. 5 key findings →
Design: longitudinal study Participants: 453 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cox regression and accelerated failure time models were used to investigate whether sex, apolipoprotein E genotype and e4 carriage were associated with amyloid onset age in all cohorts. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitive impairment without dementia is more prevalent in the United States than dementia, and its subtypes vary in prevalence and outcomes. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitive impairment is associated with increased use of health services and increased mortality. 4 key findings →
Design: cohort study Participants: 3,954 Evidence: moderate
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Insulin resistance causes diminished glucose uptake in similar regions of the brain in Alzheimer's disease (AD) and type 2 diabetes mellitus (DM2). 4 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The very mildest symptomatic stage of AD exhibits the same CSF biomarker phenotype as more advanced AD. 1 key finding →
Design: longitudinal study Participants: 139 Evidence: moderate
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Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
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.
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 31,380 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,048 records (3.3% of the library) are not peer-reviewed — 973 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →
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