28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among all participants (mean age 66.7 ± 6.5 years, 100% non-Hispanic White), 451 (6.6%) were using statins at baseline. 5 key findings →
Participants: 564 Evidence: low
Full summary, score breakdown and related studies → Original source
The PRS using 131 SNPs had an effect independent of APOE. 5 key findings →
Participants: 565 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Translating human genetic findings (genome-wide association studies [GWAS]) to pathobiology and therapeutic discovery remains a major challenge for Alzheimer's disease (AD). 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hippocampal atrophy rate has been correlated with cognitive decline and its genetic modifiers are still unclear. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We identified 11 loci-5 in H2-non-carriers and 6 in H2-carriers-although none of the MAPT haplotype-specific associations achieved genome-wide significance. 5 key findings →
Participants: 18,841 Evidence: low
Full summary, score breakdown and related studies → Original source
Extensive simulations demonstrated that the proposed approach not only provided accurate selection of single nucleotide polymorphisms (SNPs) with comparable or higher power but also robust control of false positives. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Variations in the human genome have been found to be an essential factor that affects susceptibility to Alzheimer's disease. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We propose a novel method to identify disease-related genetic variants enriched by imaging endophenotypes, which are the imaging traits associated with both genetic factors and disease status. 5 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Two novel SNPs (rs465401 and rs460420), both near the ADAMTS1 gene on chromosome 21, showed genome-wide significant associations with CSF NFL. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mild-cognitive impairment (MCI) occurs in up to one-fifth of individuals over the age of 65, with approximately a third of MCI individuals converting to dementia in later life. 2 key findings →
Participants: 122 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent genetic progress allows the molecular diagnosis of young-onset dementia, including Alzheimer's disease (AD) and frontotemporal dementia (FTD). 2 key findings →
Participants: 52 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Despite subjects with Dominantly-Inherited Alzheimer's Disease (DIAD) represent less than 1% of all Alzheimer's Disease (AD) cases, the Dominantly Inherited Alzheimer Network (DIAN) initiative constitutes a strong impact in the understanding of AD disease course with special emphasis on the presyptomatic disease phase. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most frequent diagnosis of neurodegenerative dementia with early (≤65 years) and late (>65 years) onset ages in familial and sporadic patients. 2 key findings →
Participants: 1,148 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cortical neuron loss is a pathological hallmark of late-onset Alzheimer's disease (AD). 4 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found eight flortaucipir covariance patterns which were reproducible and overlapped with relevant gene expression maps. 5 key findings →
Participants: 418 Evidence: low
Full summary, score breakdown and related studies → Original source
To assess volume loss and flortaucipir uptake in patients with semantic dementia (SD) over time. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
CL values increased significantly over the scan using the whole cerebellum, cerebellar gray matter, and brainstem as reference regions, particularly in amyloid-positive individuals. 5 key findings →
Participants: 245 Evidence: low
Full summary, score breakdown and related studies → Original source
Centiloid values significantly decreased from 52.3 ± 23.4 at baseline to - 5.6 ± 16.5 at follow-up, with a mean change of - 58.0 (p < 0.001). 5 key findings →
Participants: 12 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We examined the relationships between amyloid-β PET and concurrent and longitudinal cognitive performance in 107 cognitively normal individuals with subjective cognitive decline (age: 64 ± 8 years, 44% female, Mini-Mental State Examination score 29 ± 1). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Significantly stronger between-tracer correlations (P < .001) were observed after harmonization for both global amyloid burden indices and voxel-wise measurements in the training cohort and the external testing cohort. 3 key findings →
Participants: 92 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The combined model (Harrell's C = 0.82 [0.78-0.86]) was significantly superior to demographics (β = 0.100, P < .001), magnetic resonance imaging (β = 0.037, P = .011), and PET only models (β = 0.053, P = .003).The models can be used to calculate individualized risk, for example, a female MCI patient (age = 60, APOE ε4 positive, Mini-Mental State Examination = 25, hippocampal volume = 5.8 cm3, amyloid PET positive) has 35% (19-57) risk in one year and 85% (64-97) risk in three years. 3 key findings →
Participants: 411 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We aimed to compare [18F]-florbetaben PET imaging in four transgenic mouse strains modelling Alzheimer's disease (AD), with the main focus on APPswe/PS2 mice and C57Bl/6 mice serving as controls (WT). 1 key finding →
Design: longitudinal study Participants: 82 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Numerous studies have shown abnormal brain functional connectivity in individuals with Alzheimer's disease (AD) or amnestic mild cognitive impairment (aMCI). 1 key finding →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The results revealed abnormally increased and decreased ALFF and ReHo in PD-CN patients within the default mode network (posterior cingulate, inferior parietal cortex, parahippocampus, entorhinal cortex), sensorimotor cortex (primary motor, pre/post-central gyrus), basal ganglia (putamen, caudate), and posterior cerebellar lobule VII, which mediates cognition. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Subjective cognitive decline (SCD), as expressed by older adults, is associated with negative affect, which, in turn, is a likely risk factor for Alzheimer's Disease (AD). 5 key findings →
Design: cross-sectional Participants: 51 Evidence: low
Full summary, score breakdown and related studies → Original source
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →