Alzheimer's disease (AD) is prevalent throughout the world and is the leading cause of dementia in older individuals (aged ≥ 65 years). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is prevalent throughout the world and is the leading cause of dementia in older individuals (aged ≥ 65 years). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuropsychiatric symptoms (NPSs) are hallmarks of Alzheimer's disease (AD), causing substantial distress for both people with dementia and their caregivers, and contributing to early institutionalization. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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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In both cohorts, CSF MTBR-tau243 was associated with tau-PET temporal meta-ROI burden (BioFINDER-2: β = 1.1, p = < 0.0001 and Knight-ADRC: β = 0.7, p = < 0.0001), and this association did not differ by sex (BioFINDER-2 β = 0.04, p = 0.6 and Knight-ADRC: β = 0.009, p = 0.9). 3 key findings →
Design: cross-sectional Participants: 446 Evidence: low
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These analyses suggest that CenTauR harmonization increases the comparability of tau‐PET data acquired with different tracers. 2 key findings →
Design: longitudinal study Participants: 1,089 Evidence: moderate
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These analyses suggest that CenTauR harmonization increases the comparability of tau‐PET data acquired with different tracers. 2 key findings →
Design: longitudinal study Participants: 1,089 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. 2 key findings →
Participants: 20 Evidence: low
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Lecanemab was generally well-tolerated during the 6-month lecanemab-only treatment period. 5 key findings →
Participants: 97 Evidence: high
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CDR-SB and MoCA scores showed strong inverse correlation (Spearman's ρ = -0.68; p < 0.001). 3 key findings →
Design: cross-sectional Participants: 23,717 Evidence: moderate
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Lecanemab reduced amyloid PET in symptomatic participants with DIAD at Week 24. 3 key findings →
Participants: 97 Evidence: high
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Alzheimer's disease (AD) is the leading cause of cognitive impairment and dementia in older individuals (aged ≥ 65 years) throughout the world. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As of a data cutoff of December 3, 2024, 243 participants were screened and 197 randomized in DIAN-TU-001 Tau NexGen trial (Cohort 1: 97; Cohort 2: 100). 5 key findings →
Participants: 243 Evidence: high
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Emerging digital tools have the potential to enable a new generation of qualitative and quantitative assessment of cognitive performance. 2 key findings →
Evidence: low
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The CSF and plasma cohorts were on average 71.4(±8.5) and 72.2 (±9.3) years of age, 49.1%/50.8% was female, and 263/453 (0.59%/51.8%) were cognitively impaired, respectively. 4 key findings →
Participants: 97 Evidence: low
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< 0.0001) were significantly higher for the MCI cohort. 3 key findings →
Design: cohort study Evidence: moderate
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In CN subjects, study-wide significant (P -9 ) loci were identified for total tau near SRRM4 and C14orf79 and for hippocampal volume near MTUS1. 4 key findings →
Evidence: low
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In FFS, AD incidence (2008-2018) decreased (138 to 104); MCI incidence increased (8 to 47), but the sum (MCI + AD) was relatively stable (146 to 151). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In both cohorts there were significant associations between CSF MTBR-tau243 and the temporal meta-ROI (BioFINDER-2: t = 17.1, p < 0.001, Knight-ADRC: t=11.0, p <0.001). 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Patients (N = 2,512) receiving lecanemab infusion had a mean age of 75.4 (standard deviation = 5.7) years as compared to 80.8 (8.9) years in patients with MCI/AD not receiving the infusion. 5 key findings →
Participants: 2,512 Evidence: low
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Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The study includes symptomatic DIAD participants and asymptomatic mutation carriers. 5 key findings →
Evidence: low
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A Cognitive Task Force (CTF) was established for the MissionAD program with the aim of reducing the screen failure (SF) rate to ∼30% and thereby reduce unnecessary subject burden, site burden, and excess trial costs. 4 key findings →
Design: clinical trial Evidence: low
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Among Medicare beneficiaries from 2008 to 2018, AD prevalence was generally stable, while MCI increased. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among Medicare beneficiaries from 2008 to 2018, AD incidence generally decreased while MCI increased. 2 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.
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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events