27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease progresses heterogeneously across diverse cohorts, yet current predictive models fail to capture this complexity while remaining clinically interpretable. 4 key findings →
Design: longitudinal study Participants: 1,669 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a heterogeneous disease with many genes are associated with AD risk. 4 key findings →
Participants: 360 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is high unmet need in dementia with Lewy bodies (DLB). 4 key findings →
Participants: 159 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) pathology begins 15–20 years before clinical symptoms, necessitating non - invasive biomarkers for early diagnosis. 4 key findings →
Participants: 120 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results demonstrate that the multi-modal classifier achieved strong classification performance (accuracy = 68.64%; precision = 73.97%; F1-score=74.48%), with the highest recall (76.39%) from a model incorporating demographics and driving features, and prediction performance (accuracy = 70.48%; precision = 71.88%; F1-score = 74.80%, recall = 77.97%). 1 key finding →
Participants: 118 Evidence: low
Full summary, score breakdown and related studies → Original source
The global outbreak of COVID-19, caused by the SARS-CoV-2 virus, has been linked to long-term neurological complications, including an increased risk of Alzheimer's disease (AD) among older adults. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although human cerebellum is known to be neuropathologically impaired in Alzheimer's disease (AD) and AD-related dementias (ADRD), the cell type-specific transcriptional and epigenomic changes that contribute to this pathology are not well understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau pathology, characterized by the aberrant aggregation and accumulation of tau in neurons and glial cells, plays a critical role in the onset and progression of multiple neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study explored the role of the ubiquitin-proteasome system (UPS) in dominantly inherited Alzheimer's disease (DIAD) by examining changes in cerebrospinal fluid (CSF) levels of UPS proteins along with disease progression, AD imaging biomarkers (PiB PET, tau PET), neurodegeneration imaging measures (MRI, FDG PET), and Clinical Dementia Rating® (CDR®). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support a model in which p-tau217 specifically tracks amyloid-driven pathological progression, while markers of neurodegeneration reflect broader age-related processes that are not associated with APOE genotype. 3 key findings →
Design: longitudinal study Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The blood-based biomarker (BBM) profiles associated with genetic susceptibility to Alzheimer’s disease (AD) in general older populations remain poorly understood. 3 key findings →
Participants: 3,947 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid biomarkers sample distinct levels of an open, kinetically coupled biochemical system, yet scalar summaries may obscure biologically relevant configuration. 4 key findings →
Participants: 91 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 is elevated in αSynSAA-positive individuals at equivalent AD pathology measured by amyloid PET or the CSF ratio, and this elevation is attenuated most by fibrillar tau. 2 key findings →
Design: cross-sectional Participants: 193 Evidence: low
Full summary, score breakdown and related studies → Original source
Basal ganglia iron serves as a stage-dependent mediator linking pTau217 to hippocampal neurodegeneration, with prodromal AD potentially indicating a particularly vulnerable stage for iron-targeted interventions and iron profiling for patient stratification. 1 key finding →
Participants: 94 Evidence: low
Full summary, score breakdown and related studies → Original source
We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints. 5 key findings →
Participants: 58,876 Evidence: low
Full summary, score breakdown and related studies → Original source
Although endoplasmic reticulum (ER) stress and maladaptive unfolded protein response (UPR) are increasingly implicated in Alzheimer’s disease (AD), the influence of vitamin D (VitD) on these mechanisms remains unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
SHED exosome treatment demonstrated genotype-specific efficacy, selectively reducing p181-tau levels and restoring the p181-tau/Aβ42 ratio in FAD lines while elevating the protective Aβ42/Aβ40 ratio across both FAD and SAD backgrounds. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is a core driver of Alzheimer’s disease (AD) progression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Impaired peripheral clearance of amyloid-β (Aβ) contributes to Alzheimer's disease (AD) pathogenesis. 2 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
These data are compatible with, but do not establish, equivalence between plasma p-tau217 and CSF biomarkers. 5 key findings →
Participants: 283 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Apolipoprotein E4 (APOE4) is a major risk factor for Alzheimer’s disease (AD). 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
APOE3 Ch -associated resilience is measurably reflected in plasma biomarker trajectories, indicating attenuation of both neuroinflammatory and neurodegenerative processes. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Concordance between p-tau217 and Aβ was high in the AD and MCI groups (observed agreement 90.0% in each), but overall agreement across Cohort II was modest (166/351, 47.3%; Cohen's κ = 0.117, 95% CI 0.029–0.204). 3 key findings →
Design: longitudinal study Participants: 918 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Test-retest reliability measures are essential for interpretation of meaningful effects over time for plasma and digital outcomes. 1 key finding →
Participants: 92 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings demonstrate spatially concordant vascular and neuronal degeneration in the outer retina in preclinical AD. 3 key findings →
Design: cross-sectional 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 →