Amyloid-β (Aβ) pathology is one of the earliest detectable brain changes in Alzheimer's disease (AD) pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid-β (Aβ) pathology is one of the earliest detectable brain changes in Alzheimer's disease (AD) pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the machine learning verification, the identification accuracy of SCD, aMCI, d-AD from NC was higher when fused ALFF and fALFF features (76.44, 81.94, and 91.83%, respectively) than only using ALFF or fALFF features. 5 key findings →
Participants: 44 Evidence: low
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Our findings suggest that dCDT is a suitable screening tool to identify early cognitive dysfunction. 1 key finding →
Participants: 381 Evidence: low
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These results revealed a universal applicability of the "A/T/N" framework in a Chinese population and established an optimal diagnostic model consisting of cost-effective and non-invasive approaches for diagnosing AD. 2 key findings →
Participants: 411 Evidence: moderate
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Our results demonstrate that unsupervised digital memory assessments might be used for diagnosis and prognosis in Alzheimer's disease, potentially in combination with plasma biomarkers. 4 key findings →
Evidence: low
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The Electrophysiology Professional Interest Area (EPIA) and Global Brain Consortium endorsed recommendations on candidate electroencephalography (EEG) measures for Alzheimer's disease (AD) clinical trials. 3 key findings →
Evidence: low
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Biomarkers useful for the predementia stages of Alzheimer's disease are needed. 2 key findings →
Participants: 17 Evidence: low
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The trend changes in the hippocampus subfields and further illustrates that SCD is the preclinical stage of AD earlier than aMCI. 1 key finding →
Design: longitudinal study Evidence: moderate
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These results support the feasibility of bridging of clinical trials in the prodromal stage of AD between Asia and western countries. 3 key findings →
Participants: 75 Evidence: low
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The protein beta-amyloid is said to be central to the disease process of Alzheimer's disease (AD). 4 key findings →
Design: cross-sectional Participants: 16 Evidence: low
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We used a new method we developed for automated hippocampal segmentation, called the auto context model, to analyze brain MRI scans of 400 subjects from the Alzheimer's disease neuroimaging initiative. 4 key findings →
Participants: 400 Evidence: low
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Early diagnosis of Alzheimer's disease plays a pivotal role in patient care and clinical trials. 4 key findings →
Evidence: moderate
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The Alzheimer's Disease Neuroimaging Initiative (ADNI), launched in 2004, has worked to accelerate drug development by validating imaging and blood/cerebrospinal fluid biomarkers for Alzheimer's disease clinical treatment trials. 4 key findings →
Design: longitudinal study Evidence: moderate
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About hundred years ago, Oskar Fischer proposed that the senile plaques are the consequence of the deposition of a foreign substance that could induce an inflammatory response leading to an abnormal neuritic response of the surrounding neurons. 4 key findings →
Design: cohort study Evidence: moderate
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Baseline 18F-MK-6240 PET showed a minimal signal in CU participants, localized signal to the medial temporal lobe in participants with MCI, and a signal spanning the inferolateral temporal lobe and extending posteriorly along the ventral cortex in participants with AD. 5 key findings →
Design: longitudinal study Participants: 27 Evidence: moderate
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For detecting AD-dementia, the ensemble model achieved the area under the receiver operating characteristic curve (AUROC) of 0.943 (95% confidence interval, 0.906-0.980), 0.786 (95% confidence interval, 0.673-0.899), and 0.795 (95% confidence interval, 0.716-0.874) in the internal validation, External-1, and External-2, respectively. 4 key findings →
Design: case-control study Participants: 190 Evidence: moderate
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Our study demonstrated the robustness of a multisite Centiloid [ 11 C]PIB‐PET study and established a range of pathology‐based CL thresholds.
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Patients with mild cognitive impairment (MCI) were assessed, and a metabolic profile associated with conversion to AD at 18-month follow-up was sought.
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Mild cognitive impairment can represent a transitional state between normal ageing and Alzheimer's disease. 4 key findings →
Participants: 49 Evidence: moderate
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We observed good convergence among the 4 Good convergence was obtained among several methods for determining an optimal cutoff for 18 F-AZD4694 PET positivity. 3 key findings →
Participants: 22 Evidence: low
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Amyloid burden is an important prognostic marker in a clinically heterogeneous cohort. 5 key findings →
Evidence: moderate
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Groups were comparable on clinical and cognitive measures. 4 key findings →
Evidence: low
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Twenty-one patients with a clinical diagnosis of dementia of the Alzheimer's type (DAT) and 29 healthy, age-matched controls were studied using positron emission tomography (PET) and [18F]2-fluoro-2-deoxy-D-glucose to measure regional cerebral glucose consumption in the resting state. 3 key findings →
Evidence: low
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Registration of serial MRI volume images provides a powerful method of quantification of brain atrophy that can be used to monitor progression of AD in clinical trials. 1 key finding →
Participants: 207 Evidence: low
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Our voxel-wise results indicated that ASL-MRI provides largely overlapping information with FDG-PET. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 838 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 →