31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
To date, there is no validated fluid biomarker for tau pathology in Alzheimer's disease, with contradictory results from studies evaluating the correlation between phosphorylated tau in CSF with tau PET imaging. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among community-dwelling older adults, poorer olfaction predicts incident MCI and is associated with overall and regional Aβ. 5 key findings →
Design: cross-sectional Participants: 72 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings emphasize that treatments that remove Aβ and completely stop downstream effects on tau and neurodegeneration would only be partially effective in slowing of cognitive decline or reversing cognitive impairment. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
In two independent cohorts, t-tau and p-tau levels showed four subgroups. 2 key findings →
Participants: 1,111 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid-beta (Abeta) plays a central role in the pathogenesis of Alzheimer's disease (AD) and has been postulated as a potential biomarker for AD. 3 key findings →
Design: cross-sectional Participants: 1,032 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Systemic inflammation is associated with ischemia and Alzheimer disease (AD). 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The INNOTEST and INNO-BIA CSF platforms perform equally well in identifying individuals with underlying amyloid plaque pathology. 2 key findings →
Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our data suggest that interactions between biomarkers in AD result in a 2-phase phenomenon of pathological cortical thickening associated with low CSF Aβ, followed by atrophy once CSF p-tau becomes abnormal. 3 key findings →
Design: cross-sectional Participants: 145 Evidence: low
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CSF tau and 18 F-AV-1451 have equal performance in early clinical stages of AD, but 18 F-AV-1451 is superior in the dementia stage, and exhibits close to perfect diagnostic performance for mild to moderate AD. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Australian Imaging, Biomarkers and Lifestyle (AIBL) study performed (11)C-Pittsburgh Compound B (PiB) scans in 177 healthy controls (HC), 57 mild cognitive impairment (MCI) subjects, and 53 mild Alzheimer's disease (AD) patients. 5 key findings →
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
Full summary, score breakdown and related studies → Original source Free full text
Gold-standard diagnosis of Alzheimer's disease (AD) relies on histopathological staging systems. 3 key findings →
Participants: 159 Evidence: low
Full summary, score breakdown and related studies → Original source
This study investigated differences in retrospective cognitive trajectories between amyloid and tau PET biomarker stratified groups in initially cognitively unimpaired participants sampled from the Wisconsin Registry for Alzheimer's Prevention. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Astrocytes can adopt multiple molecular phenotypes in the brain of Alzheimer's disease (AD) patients. 4 key findings →
Participants: 121 Evidence: low
Full summary, score breakdown and related studies → Original source
Studies of rodent models of Alzheimer's disease (AD) and of human tissues suggest that the retinal changes that occur in AD, including the accumulation of amyloid beta (Aβ), may serve as surrogate markers of brain Aβ levels. 3 key findings →
Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Elevated CSF p-tau181 and cortical 18F-PI-2620 binding was characteristic for AD while normal CSF p-tau181 with elevated subcortical 18F-PI-2620 binding was characteristic for 4RTs. 18F-PI-2620-assessed posterior cortical hypoperfusion could be used as an additional neuronal injury biomarker in AD. 5 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Data were available from 131 participants with age ranging from 65.4 to 88.2 years and mean follow up of 2.4 years (SD = 1.0). 5 key findings →
Participants: 131 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain amyloid deposition is one of the main hallmarks of Alzheimer's disease (AD) and two approaches are available for assessing amyloid pathology in vivo: cerebrospinal fluid (CSF) biomarkers levels and amyloid load visualized by amyloid beta positron emission tomography imaging (Amy-PET) probes. 1 key finding →
Participants: 31 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This approach to the detection of individuals at high risk for preclinical AD-identified in single CN individuals using this quantitative ADsig MRI biomarker-may provide investigators with a population enriched for AD pathobiology and with a relatively high likelihood of imminent cognitive decline consistent with prodromal AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
[ 18 F]AV1451-PET and CSF p-tau had comparable value for differential diagnosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Systemic vascular health has significant impact on brain structure and function. 3 key findings →
Participants: 390 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Both FC-BAG and S-BAG are elevated in CI participants. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Greater intra-group heterogeneity in ATN abnormality patterns was observed in more severe clinical stages of AD. 5 key findings →
Design: cross-sectional Participants: 665 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Pathophysiologic-constrained ADL provided interpretable, personalized pathologic maps and an AI-derived ADAD score that more closely linked PET pathologic abnormalities with multimodal clinical measures. © RSNA, 2026 3 key findings →
Design: longitudinal study Participants: 7,457 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease (AD), deposition of insoluble amyloid-β (Aβ) is followed by intracellular aggregation of tau in the neocortex and subsequent neuronal cell loss, synaptic loss, brain atrophy, and cognitive impairment. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events