27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings support MRI-derived LC intensity as a marker of early AD-related processes and suggest that LC intensity may provide complementary information not captured by plasma pTau 217 alone. 4 key findings →
Design: longitudinal study Participants: 163 Evidence: moderate
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
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
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
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
DPM is fundamentally constrained by dynamic range, variability, and test–retest reliability of the biomarker of interest. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Semi-supervised multimodal fusion improves prediction and reveals interpretable imaging patterns that predict APOE4 and clinical diagnoses better than traditional approaches. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Precision medicine approaches require physiological effects to be informative when translated to the individual. 5 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source
As the only central nervous system tissue that can be directly imaged non-invasively using widely available technology, the retina offers a uniquely accessible window into the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) pathology is increasingly recognized to manifest in the retina, offering a non-invasive window for early biomarker discovery. 2 key findings →
Design: longitudinal study Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF Aβ42 rose from 526.0 to 1053.0 pg/mL (+ 100.2%), total tau (t-tau) fell from 578.2 to 278.0 pg/mL(-51.9%), and phosphorylated tau181 (p-tau181) fell from 90.8 to 23.1 pg/mL(-74.6%). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The complete absence of ARIA distinguishes XPro1595 from amyloid-targeting therapies and supports its potential for use in combination strategies and potentially for those at a higher risk of ARIA. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Electrochemical biosensors offer a promising route for the rapid, non-invasive detection of disease biomarkers by converting biochemical interactions into measurable electrical signals. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma pTau-181 demonstrates flat or declining longitudinal trajectories and minimal cognitive correlation, suggesting tau is a static biomarker rather than a dynamic therapeutic target in mid-to-late adulthood. 2 key findings →
Design: cross-sectional Participants: 2,523 Evidence: moderate
Full summary, score breakdown and related studies → Original source
DESI is a robust, fully automated MRI biomarker that sensitively detects CSF redistribution characteristic of DESH in iNPH. 1 key finding →
Design: longitudinal study Participants: 1,032 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Early, scalable detection of Alzheimer's disease (AD) and mild cognitive impairment (MCI) remains a global health priority, but non-invasive biomarkers that capture network-level dysfunction during standardized cognitive challenge remain limited. 1 key finding →
Participants: 13 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Precision psychiatry aims to identify biomarkers and develop prediction models to improve diagnosis, prognosis, and treatment selection. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Launched in 2010 by the National Institutes of Health, the Human Connectome Project (HCP) represents a foundational initiative in systems neuroscience, designed to map the structural and functional architecture of the human brain. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this prospective birth cohort study, prenatal exposure to a persistent environmental toxicant was associated with lower plasma Aβ42/40 ratio and worse cognitive performance in midlife, consistent with DDE accelerating the preclinical trajectory of AD-related biological changes decades before symptom onset. 5 key findings →
Design: cohort study Participants: 179 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) involves widespread metabolic, mitochondrial, inflammatory, and redox dysfunction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research on gut microbiota in Alzheimer’s disease (AD) has progressed from observational correlations to the validation of causal relationships. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
10 of the 2,804 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →