30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Sleep abnormalities are prevalent in Alzheimer's disease, with sleep quality already impaired at its preclinical stage. 4 key findings →
Design: cohort study Participants: 1,168 Evidence: moderate
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New technology is convenient for measuring blood total tau concentrations and provides a unique and increased opportunity for early intervention to slow cognitive decline. 4 key findings →
Design: cohort study Participants: 1,159 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Whether mild TBI (mTBI) in veterans confers a similar increased risk of AD is less known. 4 key findings →
Design: case-control study Participants: 51 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In a previous proteomic study, we identified the neurosecretory protein VGF (VGF) as a potential biomarker for dementia with Lewy bodies (DLB). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is a clear need to develop an objective diagnostic test for Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 123 Evidence: low
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There is a clear need to develop biomarkers for Parkinson disease (PD) diagnosis, differential diagnosis of Parkinsonian disorders, and monitoring disease progression. 4 key findings →
Design: cross-sectional Evidence: moderate
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Biomarkers have become increasingly important in understanding neurodegenerative processes associated with Alzheimer disease. 4 key findings →
Design: longitudinal study Participants: 116 Evidence: moderate
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Compare cognitive and hippocampal volume trajectories in asymptomatic middle-aged and older adults with positive CSF markers of β-amyloid (Aβ) or tau to adults without an Alzheimer disease (AD)-associated biomarker profile. 4 key findings →
Design: cohort study Participants: 78 Evidence: moderate
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The neuropathologic changes underlying Alzheimer disease (AD) start before overt cognitive symptoms arise, but it is not well-known how they relate to the first subtle cognitive changes. 4 key findings →
Design: cross-sectional Participants: 217 Evidence: moderate
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There are limited data regarding cerebrospinal fluid (CSF) and plasma biomarkers among patients with Cerebral Amyloid Angiopathy (CAA). 4 key findings →
Design: systematic review Evidence: high
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We investigated the effects of matrix type and reagent batch changes on diagnostic performances and longitudinal trajectories of brain-derived tau (BD-tau). 4 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
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The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →
Design: longitudinal study Participants: 350 Evidence: moderate
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Baseline CSF was collected from 512 patients with Alzheimer disease (AD) and 272 patients with other types of dementia (OD), 135 patients with a psychiatric disorder (PSY), and 275 patients with subjective memory complaints (SMC). 4 key findings →
Participants: 512 Evidence: moderate
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Phosphorylation of tau protein at threonine 231 (using full-length tau, 441 amino acids, for the numbering scheme) (p-tau(231)) occurs specifically in postmortem brain tissue of patients with Alzheimer disease (AD) and can be sensitively detected in cerebrospinal fluid (CSF). 4 key findings →
Design: cross-sectional Evidence: low
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Although advancing age is the strongest risk factor for the development of symptomatic Alzheimer disease (AD), recent studies have shown that there are individual differences in susceptibility to age-related alterations in the biomarkers of AD pathophysiology. 4 key findings →
Design: cross-sectional Participants: 268 Evidence: moderate
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Measures of neuronal loss are likely good surrogates for clinical and radiological disease progression in Alzheimer disease (AD). 4 key findings →
Design: longitudinal study Participants: 23 Evidence: moderate
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There is an urgent need to improve the understanding of neuroinflammation in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
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In this retrospective study, GAP-43 was measured in participants from the AD Neuroimaging Initiative (ADNI) cohort using an in-house ELISA method, and levels were compared between groups, both cross-sectionally and longitudinally. 4 key findings →
Participants: 786 Evidence: moderate
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Alzheimer disease (AD) is primarily associated with accumulations of amyloid plaques and tau tangles in gray matter, however, it is now acknowledged that neuroinflammation, particularly in white matter (WM), significantly contributes to the development and progression of AD. 4 key findings →
Design: cross-sectional Participants: 310 Evidence: moderate
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α-Synuclein seed amplification assays (αSAAs) can improve the diagnosis of synucleinopathies and detect α-synuclein (αSyn) copathology in vivo in clinical practice. 4 key findings →
Design: cohort study Participants: 337 Evidence: moderate
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False-positive (FP) plasma results may lead to overtreatment and false-negative (FN) results to missed or delayed disease-modifying therapies. 5 key findings →
Participants: 706 Evidence: low
Full summary, score breakdown and related studies → Original source
Virtually identical t-tau/Aβ42 cut-points (∼0.54) performed best in both test cohorts and with similar accuracy (areas under ROC curve [AUCs] [A/B: 0.95; C: 0.94]). 3 key findings →
Participants: 138 Evidence: moderate
Full summary, score breakdown and related studies → Original source
At follow-up, stage 1 subjects showed reduced atrophy rates in medial frontal areas and precuneus compared to stage 0 subjects, whereas stage 2/3 subjects presented accelerated atrophy in medial temporal structures. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Disease-modifying drug use necessitates better Alzheimer disease (AD) detection. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Accumulation of β-amyloid protein (Aβ) and tau protein is the main feature of Alzheimer disease neuropathogenesis. 4 key findings →
Participants: 35 Evidence: low
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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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 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 →
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