27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The clinical progression of Alzheimer disease (AD) is associated with the accumulation of tau neurofibrillary tangles, which may spread throughout the cortex by interneuronal tau transfer. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The unbiased amyloid, tau, and neurodegeneration (A/T/N) classification is designed to characterize individuals in the Alzheimer continuum and is currently little explored in clinical cohorts. 4 key findings →
Participants: 102 Evidence: low
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The p-tau181/Aβ 1-42 ratio showed the best prediction of Aβ-PET across all participants (area under the curve [AUC] = 0.905, 95% confidence interval [CI]: 0.86-0.95) and in CN (AUC = 0.873; 0.80-0.94), and symptomatic (AUC = 0.908; 0.82-1.00) adults. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The intraneuronal accumulation of paired helical filaments in the form of neurofibrillary tangles is one hallmark of the brain pathology in Alzheimer's disease. 4 key findings →
Evidence: low
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The study included 807 participants form K-ROAD (median age: 72.0 years, 58.7% female) and 230 from ADNI (median age: 70.9 years, 49.1% female). 5 key findings →
Design: cohort study Participants: 807 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our findings demonstrate the capability of a fingerstick collection to accurately quantify p ‐tau217 levels longitudinally and genotype ApoE. 5 key findings →
Design: longitudinal study Participants: 58 Evidence: moderate
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Older age was associated with greater odds of abnormal p-Tau217 (odds ratio [OR] 1.08 per year, 95% CI 1.07–1.09), as was APOE ε4 carrier status (OR 3.32, 95% CI 2.65–4.17). 5 key findings →
Design: cross-sectional Participants: 2,798 Evidence: moderate
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Eighty-three Black (mean 72±10.8-years-old, 63% female, 33% cognitively impaired) and 27 Latino participants (mean 65.8-years-old, 56% female, 11% cognitively impaired) completed neuroimaging. 5 key findings →
Design: longitudinal study Participants: 83 Evidence: moderate
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Plasma pTau217 levels serve as a scalable, non-invasive marker of AD-pathology across Lewy body diseases, PSP/CBS, and MCI/CU populations. 2 key findings →
Participants: 18 Evidence: low
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Aggregates of hyperphosphorylated tau (PHF-tau), such as neurofibrillary tangles, are linked to the degree of cognitive impairment in Alzheimer's disease.
Full summary, score breakdown and related studies → Original source Free full text
Aggregates of hyperphosphorylated tau (PHF-tau), such as neurofibrillary tangles, are linked to the degree of cognitive impairment in Alzheimer's disease.
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All patients underwent MRI and β-amyloid biomarker testing via 11 C-PiB or cerebrospinal fluid. 18 F-flortaucipir uptake in patients was compared to 53 β-amyloid negative normal controls using voxelwise and pre-specified region of interest approaches. 5 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
In younger controls, SUV peak was observed in the temporal lobe with values of approximately 3.0 for 11 C-RO-963, 1.5 for 11 C-RO-643, and 3.5 for 18 F-RO-948. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau-181 and GFAP are closely associated with synaptic density measured using 18 F-SynVesT-1 PET/MRI, with the relationship primarily influenced by tau accumulation rather than Aβ deposition or cortical thickness. © RSNA, 2024 Supplemental material is available for this article. 2 key findings →
Participants: 50 Evidence: low
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Our findings suggest AD-type tau is not higher in LLD compared to non-depressed, cognitively unimpaired older adults and appears unlikely to contribute to lower gray matter volume in LLD, further underscoring the need to distinguish major depressive disorder from depressive symptoms occurring in early AD. 5 key findings →
Design: cross-sectional Participants: 102 Evidence: low
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The term "aging-related tau astrogliopathy" (ARTAG) describes pathological accumulation of abnormally phosphorylated tau protein in astrocytes. 1 key finding →
Evidence: low
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We report kinetic modeling results of dynamic acquisition data from 0 to 100 min after injection with the tau PET tracer 18 F-AV-1451 in 19 subjects. 2 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The microtubule-associated protein tau is a natively unfolded protein in solution, yet it is able to polymerize into the ordered paired helical filaments (PHF) of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mutations in the microtubule-associated protein tau, including P301L, are genetically coupled to hereditary frontotemporal dementia with parkinsonism linked to chromosome 17. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF T-tau and P-tau as well as the APOE epsilon4/epsilon4 genotype are robust predictors of AD and are also associated with a more rapid progression from MCI to AD. 4 key findings →
Participants: 58 Evidence: low
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Microglia are the cells that comprise the innate immune system in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tauopathies are a class of neurodegenerative diseases marked by intracellular aggregates of hyperphosphorylated Tau. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Many neurodegenerative proteinopathies share a common pathogenic mechanism: the abnormal accumulation of disease-related proteins. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is a need for an accessible biomarker that can complement current cerebrospinal fluid and imaging biomarkers in an accurate and early diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study was undertaken to compare the performance of plasma p-tau181 with that of [ 18 F]fluorodeoxyglucose (FDG) positron emission tomography (PET) in the identification of early biological Alzheimer disease (AD). 4 key findings →
Participants: 533 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 733 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 →