31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Midlife p-tau181 was associated with faster 11-year memory decline beginning 20 years later in the ARIC cohort, which underscores a potentially long prodromal phase of cognitive decline that could precede dementia onset. 5 key findings →
Design: prospective cohort Participants: 920 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is a clear need to characterize and validate molecular biomarkers of cerebral amyloid angiopathy (CAA), in an effort to improve diagnostics, especially in the context of patients with Alzheimer disease (AD) receiving immunotherapies (for whom underlying CAA is the driver of amyloid-related imaging abnormalities). 4 key findings →
Design: meta-analysis Participants: 289 Evidence: high
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The risk of mild cognitive impairment (MCI) or dementia in individuals with subjective cognitive decline (SCD) and biomarkers indicating Alzheimer disease (AD) pathology in comparison with individuals with SCD without biomarker evidence for AD is critical to delineate the potential role of biomarker assessment in this group. 4 key findings →
Design: meta-analysis Evidence: high
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This study included patients with clinical SCD and SCD-free, healthy control (HC) participants with available baseline CSF and/or longitudinal cognitive data from the observational DZNE Longitudinal Cognitive Impairment and Dementia study. 4 key findings →
Design: longitudinal study Participants: 672 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma phosphorylated tau at threonine 181 (p-tau181), a well-validated marker of Alzheimer disease (AD) pathologic change, could be a more efficient way to diagnose AD than invasive or expensive biomarkers requiring CSF or PET. 4 key findings →
Design: cross-sectional Participants: 571 Evidence: moderate
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As a potential disease-modifying treatment for Alzheimer disease (AD), 3-amino-1-propanesulfonic acid (3APS) is a compound that binds to amyloid beta (Abeta), a toxic protein known to aggregate, leading to amyloid plaque deposition in the brain. 4 key findings →
Design: open-label trial Participants: 58 Evidence: high
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This study aimed to examine whether baseline CSF measures of Alzheimer disease (AD)-related pathology are associated with the time to onset of mild cognitive impairment (MCI) and whether these associations differ by age, sex, Apolipoprotein E ( ApoE4 ) status, and proximal (≤7 years) vs distal (>7 years) time to symptom onset. 4 key findings →
Design: longitudinal study Participants: 273 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Prion diseases can mimic Alzheimer disease (AD) at presentation. 4 key findings →
Design: cohort study Participants: 345 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitive decline associated with Parkinson disease (PD) is common and highly disabling. 4 key findings →
Design: cohort study Participants: 45 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
With the aging US population and increasing incidence of Alzheimer disease (AD), understanding factors contributing to driving cessation among older adults is crucial for clinicians. 4 key findings →
Design: longitudinal study Participants: 283 Evidence: moderate
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Dementia-related blood biomarkers are the future of large-scale dementia risk stratification; however, the extent to which phosphorylated tau (P-tau181), neurofilament light (NfL), and glial fibrillary acidic protein (GFAP) are associated with nonmodifiable risk factors has yet to be confirmed in the community, and the role of menopause has yet to be investigated. 4 key findings →
Design: cohort study Participants: 9,940 Evidence: moderate
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Core CSF changes in Alzheimer disease (AD) are decreased amyloid β(1-42), increased total tau, and increased phospho-tau, probably indicating amyloid plaque accumulation, axonal degeneration, and tangle pathology, respectively. 4 key findings →
Design: cross-sectional Participants: 529 Evidence: moderate
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Pooling data across 4 cohort studies, 814 cognitively normal participants (mean baseline age = 59.6 years) were classified into 8 ATN groups using baseline CSF levels of β-amyloid 1-42 as a measure of amyloid (A), phosphorylated tau 181 as a measure of tau (T), and total tau as a measure of neurodegeneration (N). 4 key findings →
Design: cohort study Evidence: moderate
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This study evaluated longitudinal CSF biomarker measures collected when participants were cognitively normal to determine the magnitude and time course of biomarker changes before the onset of clinical symptoms in subjects with mild cognitive impairment (MCI). 4 key findings →
Design: longitudinal study Participants: 265 Evidence: moderate
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At baseline, participants (n = 168) were cognitively normal and primarily middle-aged (mean 56.4 years, SD 10.9 years) and had both vascular risk factor status and proximal CSF biomarkers available. 4 key findings →
Design: cohort study Participants: 168 Evidence: moderate
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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
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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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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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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
We assessed whether preclinical Alzheimer disease (AD) based on CSF biomarkers at baseline predicts decline in cognitive functioning as measured by repeated neuropsychological tests for 4 cognitive domains in patients with subjective complaints. 4 key findings →
Participants: 132 Evidence: moderate
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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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 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 →
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