30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study aimed to identify lipid species associated with MPH response and explore lipid pathway disruptions in responders versus non-responders. 3 key findings →
Design: randomized controlled trial Evidence: low
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Amyloid-related imaging abnormalities (ARIA) are the principal safety concern limiting anti-amyloid therapies for Alzheimer's disease, yet their biology remains unclear. 3 key findings →
Design: case-control Participants: 3 Evidence: preliminary
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Increased UPF consumption is associated with higher risks of dementia, CIND, and CIND or dementia among US older adults. 4 key findings →
Design: cohort Participants: 5,370 Evidence: moderate
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Epilepsy was associated with higher subsequent recording of dementia and mortality over 2 years. 4 key findings →
Design: cohort study Participants: 1,812 Evidence: moderate
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Moreover, there is limited knowledge regarding associations with domain-specific cognitive decline and modifying effects of key individual characteristics. 4 key findings →
Design: cohort study Participants: 2,008 Evidence: moderate
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Late-onset unexplained epilepsy (LOUE) represents a substantial proportion of epilepsies with onset after 50 years and often manifests as temporal lobe epilepsy (LO-TLE). 4 key findings →
Design: cohort study Participants: 18 Evidence: moderate
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To efficiently implement plasma and cerebrospinal fluid (CSF) biomarkers for staging and prognosis of Alzheimer disease (AD), we must understand their dynamics across disease progression. 2 key findings →
Evidence: low
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Significant interactions between amyloid status and modifiable risk factors were observed for diabetes (adjusted β = -0.206, p = 0.032), high cholesterol (adjusted β = -0.155, p < 0.001), and physical inactivity (adjusted β = -0.161, p = 0.046), indicating combined effects rather than additive effects on cognitive decline among Aβ+ individuals. 5 key findings →
Design: cohort study Participants: 1,707 Evidence: moderate
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Across imputed data sets, a median of 2,777 eligible individuals were included, with a median of 664 receiving a new HA prescription. 5 key findings →
Evidence: high
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Due to rapid population aging, the number of Chileans with dementia is estimated to triple by 2050. 1 key finding →
Design: longitudinal study Participants: 1,778 Evidence: moderate
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Pathophysiologic-constrained ADL provided interpretable, personalized pathologic maps and an AI-derived ADAD score that more closely linked PET pathologic abnormalities with multimodal clinical measures. © RSNA, 2026 3 key findings →
Design: longitudinal study Participants: 7,457 Evidence: moderate
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Both ML short forms showed high internal consistency (α = 0.96 for ML-WHODAS-16 and 0.93 for ML-WHODAS-10) and excellent concurrent validity with the full WHODAS-32 (r = 0.98 for both). 5 key findings →
Design: longitudinal study Participants: 31,952 Evidence: moderate
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The best-performing model achieved an area under the curve of 0.86 (95% confidence interval [CI]: 0.84-0.87), with sensitivity of 73.3% (95% CI: 72.3-74.2) and specificity of 87.5% (95% CI: 86.7-88.2). 5 key findings →
Design: case-control study Participants: 8,195 Evidence: moderate
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P-tau217 demonstrated the most significant inter-group differences, the highest hazard ratio, and best distinguished MCI-Converters from MCI-Nonconverters, with its discriminative performance comparable to that of Aβ-PET measures and multi-plasma biomarker models. 5 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
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Parkinson's disease (PD) is a neurodegenerative condition that may affect both motor and cognitive function. 1 key finding →
Design: longitudinal study Participants: 115 Evidence: moderate
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Most dementias are preceded by mild cognitive impairment (MCI), a transitional clinical stage characterized by cognitive decline that does not yet significantly interfere with activities of daily living. 5 key findings →
Design: systematic review Evidence: high
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Accurate prediction of progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) is critical for early intervention. 1 key finding →
Design: longitudinal study Participants: 596 Evidence: moderate
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Regression analysis indicated that APOE ε4 non-carriers showed significantly greater improvement in MMN amplitude (β = ‒0.449, p = 0.027). 3 key findings →
Design: randomized controlled trial Participants: 21 Evidence: high
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Among 2889 patients with delirium (mean age 85 years; 54.7% female), 59.8% were triaged at SETS 1–2 (high priority) and 40.2% at SETS 3–4 (low priority). 5 key findings →
Design: cohort study Participants: 2,889 Evidence: moderate
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A total of 261 patients (75.3±6.8 years) were recruited from a memory-clinic cohort. 5 key findings →
Design: cross-sectional Participants: 261 Evidence: moderate
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Non-modifiable (age, apolipoprotein E (APOE) ɛ4 genotype and sex) and modifiable risk factors (co-morbidities at baseline, such as hypertension and cardiovascular disease, BMI, and sleep duration) were analyzed with mixed-effects models, adjusted for age and sex, to predict longitudinal measurements of WMH, Aβ and tau. 5 key findings →
Design: longitudinal study Participants: 494 Evidence: moderate
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Traumatic brain injury (TBI), a major cause of persistent cognitive impairment (CI), increases the long-term risk of developing dementia, including Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 29 Evidence: moderate
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Among nursing home residents with dementia, discontinuing long-term antipsychotic medication use was associated with lower risks of hospitalization, pneumonia, and urinary tract infections, suggesting clinical benefits in this population. 4 key findings →
Design: cohort Participants: 4,222 Evidence: moderate
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Among 356 patients (79%) with AD as the primary suspected etiology, assessment of BBM classified 149 patients (42%) as high, 101 patients (28%) as intermediate, and 106 patients (30%) as low probability of AD. 5 key findings →
Design: cohort Participants: 450 Evidence: moderate
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The results of this study indicate an AD-specific peripheral complement signature associated with disease development, highlighting complement factors as critical immune mediators that link aging and AD. 2 key findings →
Design: cohort Participants: 558 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.
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →