27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Increased levels of triglycerides at midlife predict brain Aβ and tau pathology 20 years later in cognitively healthy individuals. 5 key findings →
Design: cohort study Participants: 134 Evidence: moderate
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In older cognitively unimpaired individuals (≥50 years), widespread, age-related elevated tau signal was seen among those with normal or abnormal amyloid status as compared to younger cognitively unimpaired individuals (30-49 years). 4 key findings →
Evidence: low
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In the discovery cohort, the mean (SD) age was 70.9 (8.5) years, 191 (58%) were male, the mean (SD) MMSE score was 27.1 (1.9), and 110 individuals with MCI (33%) converted to dementia (71 to AD dementia). 4 key findings →
Design: cohort study Participants: 110 Evidence: moderate
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Among 2766 participants (mean [SD] age, 69.9 [3.8] years; 486 [17.9%] Black, 196 [7.1%] Hispanic, and 2007 [73.9%] White), 1311 developed the combined end point of MCI or dementia (849 participants with MCI and 752 participants with dementia). 5 key findings →
Design: cohort Participants: 2,766 Evidence: moderate
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Levels of plasma p-tau217 increased significantly in Aβ+ participants before showing significant deceleration (χ2 = 21.7; P Conclusions and relevance This study found that tau PET is valuable for both prognostic and real-time tracking of disease progression. 2 key findings →
Design: cohort Participants: 1,707 Evidence: moderate
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CKD was associated with increased p-tau217 concentrations when measuring p-tau217 by ALZpath and C 2 N methodologies, but the effect was mitigated by the use of %p-tau217. 5 key findings →
Design: cross-sectional Participants: 202 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Advances in molecular positron emission tomography (PET) have enabled anatomic tracking of brain pathology in longitudinal studies of normal aging and dementia, including assessment of the central model of Alzheimer's disease (AD) pathogenesis, according to which TAU pathology begins focally but expands catastrophically under the influence of amyloid-β (Aβ) pathology to mediate neurodegeneration and cognitive decline. 2 key findings →
Design: longitudinal study Participants: 104 Evidence: moderate
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Across the whole-sample, the single-modality models indicated significant correlations between the rate of cognitive decline and the first component of each imaging modality. 4 key findings →
Design: longitudinal study Participants: 12 Evidence: moderate
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For early detection of Alzheimer's disease, it is important to find biomarkers with predictive value for disease progression and clinical manifestations, such as cognitive decline. 1 key finding →
Design: longitudinal study Participants: 282 Evidence: moderate
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An increased tau positron emission tomography (PET) signal in the medial temporal lobe (MTL) has been observed in older individuals in the absence of amyloid-β (Aβ) pathology. 4 key findings →
Design: cohort study Participants: 1,093 Evidence: moderate
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This large multi-country study tested a fully automated, commercially available blood test (Lumipulse platform, measuring p-tau217) in nearly 1,800 people across memory clinics and, notably, primary care doctors' offices in Sweden, Spain, and Italy. 5 key findings →
Design: cross-sectional Participants: 1,767 Evidence: high
Full summary, score breakdown and related studies → Original source
These findings add to growing evidence that women have a differential tau response to Aβ that may emerge at the point of p-tau secretion. 5 key findings →
Design: cohort Participants: 1,292 Evidence: moderate
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In Alzheimer's disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline. 3 key findings →
Design: cohort Participants: 609 Evidence: moderate
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The BioFINDER-2 main cohort included 872 participants, with an additional 156 participants in the Knight ADRC cohort for independent validation. 2 key findings →
Design: cohort Participants: 1,028 Evidence: high
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These results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection. 4 key findings →
Design: longitudinal study Participants: 152 Evidence: moderate
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Baseline plasma VEGFA and PGF each showed a significant interaction with amyloid burden on prospective cognitive decline. 5 key findings →
Design: longitudinal study Participants: 317 Evidence: moderate
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In this randomized clinical trial, BIIB080 reduced tau biomarkers, including CSF t-tau, CSF p-tau181, and tau PET, which is associated with cognitive decline, in participants with mild AD. 5 key findings →
Design: clinical trial Participants: 13 Evidence: high
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Higher tau levels are associated with the fastest decline in everyday functioning in the presence of elevated amyloid, and those accumulating more tau show a faster decline in everyday functioning. 3 key findings →
Design: randomized controlled trial Participants: 434 Evidence: high
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Moreover, biomarker plasma levels and rates of change over time of participants who developed Alzheimer's disease dementia during follow-up were compared with age and sex-matched dementia-free control subjects. 5 key findings →
Participants: 549 Evidence: low
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In this study, elevated [18F]RO948 SUVRs were most often seen among Aβ-positive cases, which suggests that [18F]RO948 has high specificity for AD-type tau and highlights its potential as a diagnostic marker in the differential diagnosis of AD. 4 key findings →
Design: cross-sectional Participants: 257 Evidence: low
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A total of 716 individuals were included in the analysis: 413 cognitively unimpaired (CU) participants (58.6% female; mean age = 70.6 years, SD = 7.9) and 303 cognitively impaired (CI) participants (54.7% female; mean age = 73.2 years, SD = 7.4). 5 key findings →
Design: longitudinal study Participants: 716 Evidence: moderate
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Voxel-wise contrasts against controls (at P < 0.05 family-wise error corrected) showed that (18)F-AV1451 and (18)F-FDG patterns in patients with posterior cortical atrophy ('visual variant of Alzheimer's disease', n = 7) specifically targeted the clinically affected posterior brain regions, while (11)C-PiB bound diffusely throughout the neocortex. 5 key findings →
Participants: 20 Evidence: low
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In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline. 5 key findings →
Design: cohort Participants: 2,684 Evidence: high
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Aggregated insoluble tau is one of two defining features of Alzheimer's disease. 3 key findings →
Participants: 448 Evidence: low
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Higher educational level (standardized β = 0.23, P Conclusions and relevance Results of this study suggest that women and young patients with AD have relative preservation of brain structure when exposed to neocortical pathological tau. 3 key findings →
Design: cross-sectional Participants: 260 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 734 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →