The likelihood of amyloid positivity was associated with age and APOE ε4 status. 3 key findings →
Design: meta-analysis Participants: 377 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The double-cutoff approach revealed high confidence for interpreting scans as negative when Centiloid values were lower than 11 (95% CI, 9-13; I2 = 95%) and interpreting scans as positive if Centiloid values were higher than 26 (95% CI, 24-28; I2 = 95%). 3 key findings →
Design: meta-analysis Participants: 49,227 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Among the 6514 participants (mean age, 69.5 years; 50.5% female), median follow-up time ranged from 1.5 to 4.0 years. 5 key findings →
Design: longitudinal study Participants: 6,514 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Inclusion criteria included clinical diagnosis of PPA; availability of complete speech, language, and cognitive testing; magnetic resonance imaging performed within 6 months of the cognitive evaluation; and PET carbon 11-labeled Pittsburgh Compound-B or florbetapir F 18 brain scan results. 5 key findings →
Design: longitudinal study Participants: 109 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Between Feb 1, 2013, and June 28, 2019 (Barcelona), and between June 1, 2009, and Dec 31, 2014 (Cambridge), we included 388 participants with Down syndrome (257 [66%] asymptomatic, 48 [12%] with prodromal Alzheimer's disease, and 83 [21%] with Alzheimer's disease dementia) and 242 euploid controls.
Full summary, score breakdown and related studies → Original source Free full text
The impact of APOE4 on brain metabolism and structure is modified by sex. 3 key findings →
Design: cross-sectional Participants: 274 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our data suggest that [F-18]-AV-1451 holds promise as a surrogate marker for the detection of brain tau pathology in the form of tangles and paired helical filament-tau-containing neurites in Alzheimer brains but also point to its relatively lower affinity for lesions primarily made of straight tau filaments in non-Alzheimer tauopathy cases and to the existence of some [F-18]-AV-1451 off-target binding. 3 key findings →
Evidence: low
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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Individuals with DS were more likely to have microbleeds than controls (20% vs 8.9%, p 60 years) and AD clinical stage (12.42% asymptomatic, 27.9% prodromal, 35.09% dementia) were more common in APOE ε4 carriers (26% vs 18.3% noncarriers, p = 0.008), but not associated with vascular risk factors ( p > 0.05). 4 key findings →
Design: cross-sectional Participants: 276 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Low baseline Aβ42/Aβ40 was significantly associated with increased amyloid accumulation (β = 0.257, 95% confidence interval (CI) 0.177-0.336, P < 0.001), and with higher risk of conversion to Aβ-PET positivity (Hazard ratio (HR) = 2.84, 95% CI 1.14-7.04, P = 0.025) and to MCI due to AD (HR = 3.25, 95% CI 1.17-9.01, P = 0.024). 5 key findings →
Design: longitudinal study Participants: 200 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our proof-of-concept study is the first to show that microstructural and macrostructural changes can reflect underlying neuroinflammatory mechanisms in early stages of Alzheimer disease (AD). 2 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Magnetic resonance spectroscopy detects Alzheimer's disease related inflammation and neurodegeneration, and could be a good noninvasive disease-stage biomarker in Down syndrome. 3 key findings →
Participants: 118 Evidence: moderate
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51/100
The pattern of regional decreased cortical thickness that relates to cognitive deterioration is present in PD-MCI patients, involving areas that play a central role in the storage of prior experiences, integration of external perceptions, and semantic processing. 2 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A soluble fragment (sTREM2) is often found abnormally increased in cerebrospinal fluid (CSF) in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Of 822 individuals enrolled in the HEAD study, 681 participants spanning cognitively unimpaired to dementia were included. 5 key findings →
Design: cross-sectional Participants: 681 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
• Longitudinal imaging-genetics study of hippocampal atrophy trajectories over 5 years in ADNI. • APOE -ε4 carriership and ApoE CSF proteomic quantitative trait loci are key genetic drivers of accelerated hippocampal atrophy in amyloid-positive MCI. • Genetic effects are stage-specific, with strongest associations during the prodromal phase of AD. • Sex differences in atrophy rates are observed, but do not significantly alter genetic influences. • Findings support the utility of APOE and functional genetic markers as stratification tools for early neurodegeneration in AD. 4 key findings →
Design: longitudinal study Participants: 1,051 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Clinical stages showed a progressively increased prevalence of Aβ-positivity and higher entorhinal tau PET pathology from cognitively normal (CN) to SOCD, MCI, and dementia in both tracers. 5 key findings →
Design: longitudinal study Participants: 446 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
45/100
This well-characterized case of PCA syndrome due to AD in a very young patient with DS demonstrates the occurrence of atypical presentations in DS that might be overshadowed by the baseline intellectual disability associated with DS. 5 key findings →
Evidence: low
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Average age of participants was 66 (21-88) years. 25 were biologically female and 15 were amyloid positive. 5 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Average age of participants was 66 (21-88) years. 25 were biologically female and 15 were amyloid positive. 5 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In DS, PSMD changed approximately 10‐15 years before the onset of AD symptoms and linearly increased with AD clinical stages, AD pathology, and SVD metrics. 4 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid pathology in aDS individuals is linked to frontal‐predominant atrophy without clear hypometabolism. 5 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 30,980 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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