27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tau PET burden is associated with subsequent cognitive decline in Alzheimer's disease, motivating forecasts for monitoring and studies of spatially targeted therapies. 3 key findings →
Participants: 168 Evidence: low
Full summary, score breakdown and related studies → Original source
Brain positron emission tomography (PET) imaging is a valuable tool which allows visualization of the pathological structures inside the living patients’ brains. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
PVeD reproducibly contextualized associations between plasma pTau217 and PET-defined Alzheimer pathology across cohorts with different participant composition, pTau217 assays, PET tracers, and cognitive measures. 2 key findings →
Participants: 602 Evidence: low
Full summary, score breakdown and related studies → Original source
A prespecified structure–reserve–glial profile captured reproducible cognitive variation beyond measured Alzheimer disease molecular pathology across two cohorts. 1 key finding →
Design: longitudinal study Participants: 436 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Complement-mediated neuroinflammation has been implicated in Alzheimer’s disease (AD), but its role during the pre-symptomatic phase of the disease remains unclear. 4 key findings →
Participants: 708 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid-β and tau, pathological hallmarks of AD, silently accumulate years before clinical symptoms’ onset and are associated with neuronal dysfunction and cognitive impairment. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The medial temporal lobe (MTL) is crucial for episodic memory. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain perfusion SPECT revealed AD-typical hypoperfusion patterns and demonstrated modest potential to estimate the presence or absence of Aβ deposition with left parietal rCBF. 5 key findings →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) pathology develops years in advance prior to its clinical presentation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ninety-six non-artifactual Amyloid-Tau components were identified, of which 73 showed appreciable spatial correspondence between their paired Amyloid and Tau maps, while 17 were Tau-localized and 6 Amyloid-localized. 2 key findings →
Participants: 320 Evidence: low
Full summary, score breakdown and related studies → Original source
This study investigated whether WM measures derived from amyloid-PET are associated with AD biomarkers and to determine whether they offer added diagnostic and prognostic value beyond established biomarkers. 5 key findings →
Participants: 320 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid regional extent and tau PET were associated with different features of dyadic CFI data: reporter balance and CFI burden across reporters, respectively. 4 key findings →
Design: cross-sectional Participants: 1,686 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Event-based models (EBMs) are used to infer ordering of biomarker alteration patterns with respect to disease progression. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Diffusion MRI (dMRI) enables assessment of white matter microstructural abnormalities in Alzheimer's disease (AD), and multisite datasets enable more robust modeling of non-biological variation that can confound analyses. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
RNT was associated with increasing global amyloid accumulation even after controlling for psychological symptoms (B = 0.0120, 95% Confidence Interval 0.003 to 0.021, P = 0.012), and in sensitivity analyses limited to participants aged ≥50 or ≥60. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Foundation models have driven major advancements in the language and vision domains, as seen in the popularity of Artificial Intelligence (AI) tools, and a growing number of studies are bringing the approach to human brain imaging. 2 key findings →
Participants: 343 Evidence: low
Full summary, score breakdown and related studies → Original source
A continuous amyloid staging score complements global amyloid burden for early AD staging and cognitive risk stratification. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
: Treated patients were 74±7 years old; 57% were female, 59% were apolipoprotein E ε4 carriers, and 78% had mild cognitive impairment (22% mild dementia). 5 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Of 204 normative reference models, 199 (97.5%) met the predefined diagnostic criteria; median held-out explained variance (EXPV) was 0.174. 2 key findings →
Design: longitudinal study Participants: 111 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Aging is the greatest risk factor for Alzheimer's disease (AD), yet how and when AD-related pathological progression diverges from aging remains poorly understood. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease pathology and cognitive outcomes frequently diverge, yet current single-axis definitions cannot identify resilient (high pathology, preserved cognition) and resistant (high risk, low pathology) subgroups reliably at scale, obscuring the mechanisms that uncouple pathological burden from cognitive decline. 2 key findings →
Participants: 1,009 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease and cerebral amyloid angiopathy are characterized by the accumulation of amyloid-β (Aβ) species, yet the human fluid-physiological mechanisms that regulate soluble Aβ transport and clearance remain poorly understood. 3 key findings →
Participants: 502 Evidence: moderate
Full summary, score breakdown and related studies → Original source
As the world's population ages, Alzheimer's disease (AD), a progressive neurodegenerative disorder, is becoming more common. 1 key finding →
Participants: 59 Evidence: low
Full summary, score breakdown and related studies → Original source
Residualized WMH T1w/T2w-FLAIR ratio captures lesion-specific microstructural variation missed by volumetric measures, consistent with vascular-gliotic injury in VD and coexisting amyloid-linked demyelination in AD. 4 key findings →
Design: cross-sectional Participants: 71 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Structured Abstract INTRODUCTION Alzheimer’s disease (AD) progresses over decades, yet plasma biomarkers that resolve disease stage rather than simply detect disease remain scarce. 3 key findings →
Participants: 90 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 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 →