27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Unlike the CSF biomarkers evaluated, changes in serial structural MRI are correlated with concurrent change on general cognitive and functional indices in impaired subjects, track with clinical disease stage, and are influenced by APOE genotype. 3 key findings →
Participants: 312 Evidence: low
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An a priori defined cutoff value of p-tau(231) yields relatively stable results across centers, suggesting a good feasibility of a standard criterion of p-tau(231) for the prediction of Alzheimer disease. 2 key findings →
Participants: 43 Evidence: low
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The current study suggests that lower Abeta 42 levels reflect neuropathologic processes implicated in amyloid-related pathologies, such as NP and CAA. 3 key findings →
Evidence: low
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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
Mean plasma Abeta40 levels were higher in the AD group than in controls (P = .005), but there was substantial overlap; Abeta42 levels were similar between the groups. 4 key findings →
Participants: 78 Evidence: low
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Several potential disease-modifying drugs for Alzheimer's disease (AD) have failed to show any effect on disease progression in clinical trials, conceivably because the AD subjects are already too advanced to derive clinical benefit from treatment and because diagnosis based on clinical criteria alone introduces a high misdiagnosis rate. 1 key finding →
Evidence: low
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Reliable blood biomarkers for Alzheimer's disease (AD) are missing. 1 key finding →
Participants: 28 Evidence: low
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Tau form ratio was significantly reduced in patients with PSP (0.504 +/- 0.284) when compared to age-matched controls (0.989 +/- 0.343), and to patients with other neurodegenerative conditions (range = 0.899-1.215). 2 key findings →
Participants: 166 Evidence: low
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Black Americans are disproportionately affected by dementia. 3 key findings →
Evidence: low
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No large-scale characterizations of neurofilament light chain (NfL) have been conducted in diverse populations. 1 key finding →
Participants: 890 Evidence: low
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As a result, our combined method achieved an area under the receiver operating characteristic (AU-ROC) curve of 98.33, 93.59, 96.83, 94.64, 96.43, and 95.24% for AD vs. MCIs subjects which are high relative to single modality results and other state-of-the-art approaches. 2 key findings →
Participants: 158 Evidence: low
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The findings suggest that GPS driving may serve as an effective and accurate digital biomarker for identifying preclinical AD among older adults. 2 key findings →
Participants: 64 Evidence: moderate
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Precision medicine for Alzheimer's disease (AD) necessitates the development of personalized, reproducible, and neuroscientifically interpretable biomarkers, yet despite remarkable advances, few such biomarkers are available. 1 key finding →
Participants: 716 Evidence: low
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Digital biomarker prognostic models can be a useful tool to assist large-scale population screening for the early detection of cognitive impairment and patient monitoring over time. 1 key finding →
Design: longitudinal study Evidence: moderate
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Accurate early diagnosis of neurodegenerative diseases represents a growing challenge for current clinical practice. 5 key findings →
Participants: 200 Evidence: moderate
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Patients with Alzheimer's disease (AD) have elevations of fasting plasma insulin that are hypothesized to be associated with disrupted brain insulin metabolism. 2 key findings →
Participants: 25 Evidence: low
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Patients with isolated rapid-eye-movement sleep behaviour disorder (RBD) are commonly regarded as being in the early stages of a progressive neurodegenerative disease involving α-synuclein pathology, such as Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy. 1 key finding →
Evidence: low
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Almost all individuals with Down Syndrome (DS) develop Alzheimer's disease (AD) by mid to late life. 3 key findings →
Participants: 229 Evidence: moderate
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The discovery and reliable detection of markers for neurodegenerative diseases have been complicated by the inaccessibility of the diseased tissue--such as the inability to biopsy or test tissue from the central nervous system directly. 2 key findings →
Participants: 69 Evidence: low
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By fitting Cox proportional hazards models, we find that baseline model stage is a significant risk factor for conversion from both mild cognitive impairment to Alzheimer's disease (P = 2.06 × 10(-7)) and cognitively normal to mild cognitive impairment (P = 0.033). 2 key findings →
Evidence: low
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We developed an accurate prognostic model for predicting MCI-to-dementia progression over a three-year period. 4 key findings →
Participants: 139 Evidence: low
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Neuroinflammation has gained increasing attention as a potential contributing factor in Alzheimer's disease (AD) pathology. 4 key findings →
Participants: 399 Evidence: moderate
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In Alzheimer's disease (AD), tau phosphorylation in the brain and its subsequent release into cerebrospinal fluid (CSF) and blood is a dynamic process that changes during disease evolution. 4 key findings →
Evidence: low
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Both low and high body mass index (BMI) has been associated with cognitive impairment and dementia risk, including Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 101 Evidence: low
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Cerebrospinal fluid (CSF) biomarkers have been used to increase the evidence of underlying Alzheimer's disease (AD) pathology in mild cognitive impairment (MCI). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 2,804 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →