27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Bapineuzumab did not improve clinical outcomes in patients with Alzheimer's disease, despite treatment differences in biomarkers observed in APOE ε4 carriers. 1 key finding →
Design: clinical trial Participants: 1,090 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Following reports of meningoencephalitis (overall 18/300 [6%]), immunization was stopped after one (2 patients), two (274 patients), or three (24 patients) injections. 3 key findings →
Participants: 300 Evidence: high
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Two hundred eighty-eight patients had paired scans (mean interval 10.9 months). 2 key findings →
Participants: 45 Evidence: high
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Significant proportions of the observed variance in age at symptom onset in ADAD can be explained by family history and mutation type, providing empirical support for use of these data to estimate onset in clinical research. 2 key findings →
Participants: 3,275 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
No significant differences were found in the primary efficacy analysis. 2 key findings →
Design: clinical trial Participants: 234 Evidence: low
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Infusion of bapineuzumab 0.5 or 1.0 mg/kg every 13 weeks for up to 3 years was generally well tolerated, with a safety and tolerability profile similar to that in previous studies. 3 key findings →
Participants: 1,462 Evidence: low
Full summary, score breakdown and related studies → Original source
Baseline biomarkers largely do not predict risk for developing ARIA-E. ARIA-E was associated with significant longitudinal changes in several biomarkers, with larger reductions in amyloid PET and CSF p-tau and t-tau concentrations, and paradoxically greater hippocampal volume reduction and ventricular enlargement, suggesting that ARIA-E in bapineuzumab-treated cases may be related to increased Aβ efflux from the brain and affecting downstream pathogenic processes. 4 key findings →
Design: longitudinal study Participants: 1,512 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitive decline and dementia incidence have also been consistently associated with exposure to air pollution. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
See Li and Donohue (doi:10.1093/brain/awy089) for a scientific commentary on this article. 4 key findings →
Design: longitudinal study Participants: 338 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This expert commission synthesized decades of population-level (observational) research to estimate how much dementia risk could theoretically be reduced by addressing 14 modifiable risk factors across life, from childhood education to late-life social isolation. 3 key findings →
Design: systematic-review Evidence: moderate
Full summary, score breakdown and related studies → Original source
Medial temporal lobe atrophy seems to be a more important predictor of cognition than small-vessel disease in MCI. 4 key findings →
Design: cohort study Participants: 896 Evidence: high
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An optimized immunoassay was used to analyze CSF Ng in a retrospective cohort of 331 participants with different neurodegenerative diseases, including healthy controls (n = 19), biomarker-proven Alzheimer disease (AD) (n = 100), genetic AD (n = 2), behavioral variant frontotemporal dementia (n = 20), speech variant frontotemporal dementia (n = 21), Lewy body dementia (n = 13), Parkinson disease (n = 31), progressive supranuclear palsy (n = 46), multiple system atrophy (n = 29), as well as a heterogeneous group with non-neurodegenerative cognitive impairment (n = 50). 1 key finding →
Design: retrospective cohort Participants: 19 Evidence: moderate
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Rates of hippocampal atrophy (%/year) were 0.0 +/- 0.8 in the absent, 1.7 +/- 0.4 in the moderate, and 3.6 +/- 1.0 in the severe (mean +/- SD) tertile. 2 key findings →
Participants: 323 Evidence: moderate
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We used Kaplan-Meier survival analysis to examine the distribution of incident ARIA-E from the start of bapineuzumab treatment and proportional hazards regression models to assess risk factors associated with ARIA. 3 key findings →
Design: clinical trial Participants: 262 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease is associated with progressive cerebral atrophy, which can be seen on MRI with high resolution. 2 key findings →
Design: longitudinal study Evidence: moderate
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To be diagnostically useful, structural MRI must reliably distinguish Alzheimer's disease (AD) from normal aging in individual scans. 1 key finding →
Evidence: low
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Mutation carriers had significantly increased hippocampal and whole-brain atrophy rates compared with controls and these differences increased with time. 2 key findings →
Design: cross-sectional Evidence: moderate
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A panel of nine CSF biomarkers was able to differentiate APS from patients with PD and dementia. 2 key findings →
Design: prospective cohort Participants: 31 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Whole brain atrophy rate discriminates Alzheimer disease (AD) from MCI. 1 key finding →
Participants: 64 Evidence: low
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The extent to which cerebral atrophy in Alzheimer's disease changes with time is unknown. 4 key findings →
Participants: 12 Evidence: low
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MRI can also be used to assess comorbid vascular pathology and define homogeneous groups for inclusion or for subject stratification. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Structural imaging based on magnetic resonance is an integral part of the clinical assessment of patients with suspected Alzheimer dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
By fitting Cox proportional hazards models, we find that baseline model stage is a significant risk factor for conversion from both mild cognitive impairment to Alzheimer's disease (P = 2.06 × 10(-7)) and cognitively normal to mild cognitive impairment (P = 0.033). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The hippocampal formation (HF) is known from pathological and MRI studies to be severely atrophied in established Alzheimer's disease. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Posterior cortical atrophy (PCA) is a neurodegenerative syndrome that is characterised by progressive decline in visuospatial, visuoperceptual, literacy, and praxic skills. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% of the library) are not peer-reviewed — 962 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 →