27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Identifying concomitant Lewy body (LB) pathology through seed amplification assays (SAA) might enhance the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice and trials. 2 key findings →
Design: cohort Participants: 795 Evidence: moderate
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These data support the use of cNfL as a biomarker of neuroaxonal damage and indicate that age-specific and sex-specific (and in some cases disease-specific) reference values may be needed. 4 key findings →
Participants: 2,795 Evidence: moderate
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Non-pharmacological therapies, such as physical activity interventions, are an appealing alternative or add-on to current pharmacological treatment of cognitive symptoms in patients with dementia. 4 key findings →
Design: meta-analysis Participants: 802 Evidence: high
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Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic workup of dementia in clinical practice and the design of clinical trials. 4 key findings →
Design: longitudinal study Participants: 426 Evidence: moderate
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The BioFINDER-2 main cohort included 872 participants, with an additional 156 participants in the Knight ADRC cohort for independent validation. 2 key findings →
Design: cohort Participants: 1,028 Evidence: high
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Alzheimer's disease (AD), the leading cause of dementia, has an estimated heritability of approximately 70% 1 . 3 key findings →
Participants: 32,558 Evidence: low
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Voxel-wise contrasts against controls (at P < 0.05 family-wise error corrected) showed that (18)F-AV1451 and (18)F-FDG patterns in patients with posterior cortical atrophy ('visual variant of Alzheimer's disease', n = 7) specifically targeted the clinically affected posterior brain regions, while (11)C-PiB bound diffusely throughout the neocortex. 5 key findings →
Participants: 20 Evidence: low
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Aggregated insoluble tau is one of two defining features of Alzheimer's disease. 3 key findings →
Participants: 448 Evidence: low
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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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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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In this genetic association study, a novel variant associated with AD was identified: R251G always coinherited with ε4 on the APOE gene, which mitigates the ε4-associated AD risk. 5 key findings →
Design: case-control study Participants: 37 Evidence: moderate
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The aim of this international guideline on dementia was to present a peer-reviewed evidence-based statement for the guidance of practice for clinical neurologists, geriatricians, psychiatrists, and other specialist physicians responsible for the care of patients with dementia. 1 key finding →
Design: meta-analysis Evidence: high
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Patients with FTLD were distributed between FTLD-tau (34 patients: 10 corticobasal degeneration, nine progressive supranuclear palsy, eight Pick's disease, three frontotemporal dementia with parkinsonism associated with chromosome 17, three unclassifiable tauopathy, and one argyrophilic grain disease); FTLD-TDP (55 patients: nine type A including one with motor neuron disease, 27 type B including 21 with motor neuron disease, eight type C with right temporal lobe presentations, and 11 unclassifiable including eight with motor neuron disease), FTLD-FUS (eight patients), and one patient with FTLD-ubiquitin proteasome system positive inclusions (FTLD-UPS) that stained negatively for tau, TDP-43, and FUS. 4 key findings →
Participants: 438 Evidence: moderate
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Our findings suggest that tau PET is more sensitive than Aβ PET and measures of cortical thickness for detecting early cognitive changes in preclinical AD. 2 key findings →
Design: cross-sectional Participants: 106 Evidence: low
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In patients with sporadic ALS, we identified the repeat expansion in 236 (7·0%) of 3377 white individuals from the USA, Europe, and Australia, two (4·1%) of 49 black individuals from the USA, and six (8·3%) of 72 Hispanic individuals from the USA. 1 key finding →
Participants: 4,448 Evidence: low
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The CSF AD profile was more common in patients with SCI (31 of 60 [52%]), naMCI (25 of 37 [68%]), and aMCI (56 of 71 [79%]) than in healthy controls (28 of 89 [31%]). 3 key findings →
Design: cohort study Evidence: moderate
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Main results We identified no studies which met the inclusion criteria. 1 key finding →
Design: systematic review Evidence: high
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The SCIENCe study confirms that SCD is a heterogeneous group, with preclinical AD and subthreshold psychiatric features. 4 key findings →
Design: cohort study Participants: 114 Evidence: moderate
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The APOE-ε4 allele is associated with a moderately increased risk for progression from MCI to AD-type dementia. 4 key findings →
Design: meta-analysis Participants: 35 Evidence: high
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Understanding the neuropathological effects of amyloid β (Aβ)-targeting therapies and amyloid-related imaging abnormalities (ARIA) in Alzheimer's disease is critical for optimising treatment efficacy and patient outcomes. 4 key findings →
Design: case-control study Evidence: moderate
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Insoluble tau aggregates within neurofibrillary tangles are a defining neuropathological feature of Alzheimer’s disease (AD) and closely correlate with clinical symptoms. 2 key findings →
Participants: 108 Evidence: low
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Researchers performed a genome-wide association study of clinically diagnosed Alzheimer's disease and disease-by-proxy. 3 key findings →
Evidence: low
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Of 386 participants, 199 (52%) were female, and the mean (SD) age was 68 (8) years. 3 key findings →
Design: cohort study Participants: 113 Evidence: moderate
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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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In total, 1,234 articles were identified from the search; 21 articles met inclusion criteria. 5 key findings →
Design: systematic review Evidence: high
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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →