31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma p-tau217 and tau positron emission tomography (PET) are strong prognostic biomarkers in Alzheimer's disease (AD), but their relative performance in predicting future cognitive decline among cognitively unimpaired (CU) individuals is unclear. 2 key findings →
Design: cohort Participants: 1,474 Evidence: high
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Mean age was 83.5 (SD, 8.5) years in cohort 1, 69.1 (SD, 10.3) years in cohort 2, and 35.8 (SD, 10.7) years in cohort 3; 38% were women in cohort 1, 51% in cohort 2, and 57% in cohort 3. 4 key findings →
Design: cross-sectional Participants: 301 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among 1431 participants, the mean (SD) age was 71.2 (8.8) years; 751 (52.5%) were male. 2 key findings →
Design: cohort study Participants: 1,135 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A major unanswered question in the dementia field is whether cognitively unimpaired individuals who harbor both Alzheimer's disease neuropathological hallmarks (that is, amyloid-β plaques and tau neurofibrillary tangles) can preserve their cognition over time or are destined to decline. 3 key findings →
Participants: 1,325 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified that combining plasma p-tau217 and a brief cognitive composite score was strongly related to greater risk of progression to AD dementia in MCI patients, suggesting that these measures could be key components of future prognostic algorithms for early AD. 2 key findings →
Participants: 110 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau181 (P-tau181) might be increased in Alzheimer's disease (AD), but its usefulness for differential diagnosis and prognosis is unclear. 2 key findings →
Participants: 589 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Plasma levels of tau phosphorylated at threonine-217 (p-tau217) is a candidate tool to monitor Alzheimer's disease. 2 key findings →
Design: longitudinal study Participants: 62 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Participants had a mean (SD) age of 66.9 (9.9) years; 971 (33.3%) were Aβ positive by either CSF or PET, 1667 (57.2%) were women, and 1108 (38.1%) carried at least 1 APOE ε4 allele. 5 key findings →
Design: cross-sectional Participants: 2,916 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The best CSF measures for identifying MCI-AD were Aβ42/total tau (t-tau) and Aβ42/hyperphosphorylated tau (p-tau) (area under the curve [AUC] 0.93-0.94). 3 key findings →
Design: longitudinal study Participants: 122 Evidence: moderate
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A combination of plasma phospho-tau (P-tau) and other accessible biomarkers might provide accurate prediction about the risk of developing Alzheimer's disease (AD) dementia. 2 key findings →
Participants: 340 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found that accelerated increase in tau-PET signal was observed in amyloid-β-positive mild cognitive impairment (3.0 ± 5.3%) and Alzheimer's disease dementia (2.9 ± 5.7%), respectively, when compared to either amyloid-β-negative cognitively unimpaired (0.4 ± 2.7%), amyloid-β-negative mild cognitive impairment (-0.4 ± 2.3%) or amyloid-β-positive cognitively unimpaired (1.2 ± 2.8%). 4 key findings →
Design: cohort study Participants: 157 Evidence: moderate
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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
Full summary, score breakdown and related studies → Original source Free full text
Our findings show that different AT(N) variants are not interchangeable, and that optimal variants differ by clinical stage. 4 key findings →
Design: longitudinal study Participants: 490 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Most neuroinflammatory CSF biomarkers were associated with WML in individuals without dementia. 5 key findings →
Design: longitudinal study Participants: 247 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our findings suggest that tau PET is more sensitive than Aβ PET and measures of cortical thickness for detecting early cognitive changes in preclinical AD. 2 key findings →
Design: cross-sectional Participants: 106 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We developed models for individualized risk prediction of cognitive decline in mild cognitive impairment (MCI) using plasma biomarkers of β-amyloid (Aβ), tau and neurodegeneration. 4 key findings →
Design: longitudinal study Participants: 573 Evidence: moderate
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Impaired spatial navigation was associated with conversion to dementia within 2 and 4 years and with key CSF and MRI biomarkers for AD and neurodegeneration in patients with SCD and MCI. 5 key findings →
Design: cohort study Participants: 176 Evidence: moderate
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Implementation of amyloid biomarkers in clinical practice would be accelerated if such biomarkers could be measured in blood. 4 key findings →
Participants: 719 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease, post-mortem studies have shown that the first cortical site where neurofibrillary tangles appear is the transentorhinal region, a subregion within the medial temporal lobe that largely overlaps with Brodmann area 35, and the entorhinal cortex. 5 key findings →
Participants: 215 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The high accuracies for Aβ pathology and future AD dementia using fully automated instruments are promising for implementing plasma biomarkers in clinical trials and clinical routine. 2 key findings →
Participants: 920 Evidence: low
Full summary, score breakdown and related studies → Original source
We identified several demographic, clinical, and neurobiological factors that are important to explain the variance in tau PET retention observed across the AD pathological continuum, non-AD neurodegenerative disorders, and cognitively unimpaired persons. 1 key finding →
Participants: 1,944 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers of amyloid, tau, and neurodegeneration (ATN) need to be characterized in cognitively unimpaired (CU) elderly individuals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A combination of plasma Aβ42/Aβ40 and p-tau217 discriminated Aβ status with relatively high accuracy, whereas p-tau217 showed strongest associations with Aβ pathology in MCI but not in CU. 1 key finding →
Participants: 591 Evidence: low
Full summary, score breakdown and related studies → Original source
It is unknown how neuroinflammation may feature in the etiology of Alzheimer's disease (AD). 1 key finding →
Participants: 1,291 Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic pathways implicated in causing AD are related to altered levels of soluble tau through both Aβ-dependent and Aβ-independent mechanisms, which may have relevance for anti-tau drug development. 3 key findings →
Participants: 751 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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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