27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Second, we examined volumetric associations with amyloid (amyloid positive, tau negative versus control) and tau in the presence of amyloid (amyloid positive, tau positive versus amyloid positive, tau negative) across 52 brain areas. 5 key findings →
Design: meta-analysis Participants: 306 Evidence: high
Full summary, score breakdown and related studies → Original source
An accurate blood test for Alzheimer's disease that is sensitive to preclinical proteinopathy and cognitive decline has clear implications for early detection and secondary prevention. 2 key findings →
Design: cohort study Participants: 165 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We demonstrated that higher amyloid burden as measured by both CSF amyloid beta 42/40 ratio and non-displaceable binding potential in the posterior cingulate cortex was associated with lower functional connectivity in the default mode network. 3 key findings →
Design: longitudinal study Participants: 173 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mixed-effect models assessed rates of memory decline in relation to baseline plasma p-tau181, and whether plasma p-tau181 significantly predicted memory decline beyond widely available clinical and genetic data (age, sex, years of education, cardiovascular and metabolic conditions, and APOEε4 status). 5 key findings →
Design: longitudinal study Participants: 604 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma amyloid-β peptide concentration has recently been shown to have high accuracy to predict amyloid-β plaque burden in the brain. 2 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The chronological progression of brain atrophy over decades, from pre-symptomatic to dementia stages, has never been formally depicted in Alzheimer's disease. 2 key findings →
Design: cross-sectional Participants: 3,512 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study tracked tau PET scans over time in over 800 people across the Alzheimer's spectrum and found that while tau broadly follows the classic 'Braak stage' spreading pattern, the exact regions affected vary a lot from person to person, especially as disease progresses. 4 key findings →
Design: cohort Participants: 832 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Regions with early signs of elevated amyloid β uptake were used to form an early, focal composite and compared to a commonly used global composite, in a separate validation sample. 3 key findings →
Design: longitudinal study Participants: 279 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma phosphorylated tau217 has been suggested as a core biomarker for establishing a biological Alzheimer's disease diagnosis. 2 key findings →
Design: cross-sectional Participants: 691 Evidence: low
Full summary, score breakdown and related studies → Original source
In multivariable analyses, none of the plasma biomarkers were significantly associated with cognitive impairment. 5 key findings →
Participants: 403 Evidence: low
Full summary, score breakdown and related studies → Original source
Although recent studies have demonstrated the prognostic utility of plasma biomarkers of Alzheimer pathology or neurodegeneration, such as pTau-181 and NF-L, whether other plasma biomarkers can further improve prediction of cognitive decline is undetermined. 5 key findings →
Design: cohort study Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We used within-group locally estimated scatterplot smoothing models to compare the trajectory of biomarker changes with age in females versus males, as well as by apolipoprotein ɛ4 carriership. 5 key findings →
Design: cross-sectional Participants: 628 Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep abnormalities are prevalent in Alzheimer's disease, with sleep quality already impaired at its preclinical stage. 4 key findings →
Design: cohort study Participants: 1,168 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
NEFL (hazard ratio [HR] [95% confidence intervals (CIs)]: 1.54 [1.29, 1.84]) and RPS6KB1 (HR [95% CI]: 1.33 [1.16, 1.52]) were robustly associated with incident all-cause dementia; MMP12 (HR [95% CI]: 2.06 [1.41, 2.99]) was associated with vascular dementia in ELSA, after correcting for multiple testing. 3 key findings →
Design: longitudinal study Participants: 3,249 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Individuals with autosomal dominant frontotemporal dementia (FTD) exhibit considerable variability in disease onset and progression. 5 key findings →
Participants: 711 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Although, anatomical disparities of the rodent medial prefrontal cortex compared to the primate homologue are apparent, current rodent models have effectively implicated the medial prefrontal cortex as a neural substrate of cognitive decline within ageing and dementia. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There was a direct and indirect bidirectional effect through the glial fibrillary acidic protein of WMH on phosphorylated tau 217 concentration, which was associated with neurofilament light chain concentration in the entire sample. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Reduced within-network connectivity was observed in the language network in both phenotypes, with stronger evidence of reductions in logopenic progressive aphasia compared to controls. 5 key findings →
Participants: 144 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Digital cognitive testing using online platforms has emerged as a potentially transformative tool in clinical neuroscience. 3 key findings →
Participants: 325 Evidence: low
Full summary, score breakdown and related studies → Original source
Fusion of all five data modalities (n = 111) yielded two subtypes (n S1 = 53, n S2 = 58), which were nominally associated with diffuse amyloid plaques; however, this effect was not significant after correction for multiple testing. 5 key findings →
Participants: 111 Evidence: low
Full summary, score breakdown and related studies → Original source
A subset of participants received cognitive testing and/or the Movement Disorders Society Unified Parkinson's Disease Rating Scale Part III motor exam (off medication). 18F-PI-2620 uptake was low overall in Lewy body disease and correlated with β-amyloid PET in temporal lobe regions and precuneus. 5 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies have explored the associations of retinal vessel calibre, measured from retinal photographs or fundus images using semi-automated computer programs, with cognitive impairment and dementia, supporting the concept that retinal blood vessels reflect microvascular changes in the brain. 3 key findings →
Participants: 212 Evidence: low
Full summary, score breakdown and related studies → Original source
Higher grey matter volumes/cortical thickness and fluorodeoxyglucose uptake have been consistently found in cognitively unimpaired individuals with abnormal Alzheimer's disease biomarkers compared with those with normal biomarkers. 4 key findings →
Participants: 319 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
For amyloid positive individuals Aβ42/Aβ40, glial fibrillary acidic protein and p-tau181 were the top predictors of cognitive decline while Aβ42/Aβ40 was prominent for amyloid negative participants across all age groups. 5 key findings →
Design: cross-sectional Participants: 1,185 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Given that cognitive performance in the A-/T+ group was poorer than in individuals without either pathology, our results suggest that medial temporal lobe tau without cortical amyloid beta may reflect an early stage on the Alzheimer's pathological continuum. 1 key finding →
Participants: 301 Evidence: low
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 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 →