27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurodegenerative proteinopathies are defined by distinct proteins whose folding, trafficking and clearance depend on shared proteostasis machinery. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apigenin is an abundant, bioactive phytochemical with reported therapeutic potential and neuroprotective effects in a variety of age-related disease models. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Environmental microplastics and nanoplastics (MNPs) are emerging contaminants that accumulate in human tissues, including the brain, yet their mechanistic impact on the nervous system remains poorly understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is characterised by aberrant amyloid beta and tau aggregation, neuroinflammation, demyelination and neurodegeneration, which have been linked to changes in cell-specific gene expression signatures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although dementias primarily affect memory, they also disrupt our closest social relationships, resulting in elevated caregiver burden and worse patient outcomes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Structured Abstract Background Alzheimer’s disease (AD) neuropathology emerges decades before symptoms, requiring sensitive, non-invasive markers for early diagnosis. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) target evidence is distributed across biological, chemical, structural, regulatory, and trial-registry sources, complicating reproducible target evaluation and modeling. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
To distinguish these cases, we trained three types of supervised 3D transformers (ViT3D, MINiT, NIT) and, as a non-collapsing alternative, a frozen self-supervised encoder (DINO), to classify people with dementia or mild cognitive impairment (MCI) versus cognitively normal (CN) individuals from 3D brain MRI, using data from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A bstract Deep learning models for electroencephalography (EEG) pathology detection achieve competitive accuracy but offer limited interpretability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroimaging studies that pool data across clinical sites often suffer from site effects — variability in imaging measures that arises from technical heterogeneity across sites as opposed to true biological signal. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Alzheimer’s Disease Neuroimaging Initiative (ADNI) is widely used to train machine learning models for Alzheimer’s disease, yet whether it provides consistent ground truth for predictive modeling has not been systematically tested. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Immunofluorescence staining of FFPE tissue following Xenium processing also preserves cellular morphology, allowing the morphological complexity of distinct cell types to be captured and quantitated, especially for glial cells with highly ramified processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Subcortical brain alterations are a key feature of dementia disease progression. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The reproducibility crisis in biomedical research calls for re-evaluation of how common analytic approaches affect results. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Validated on synthetic ground truth, the audit separates a generalizable anchor (PTGDS) from a dataset-specific signal and a global-expression artefact, providing a reusable control for trajectory-based molecular staging. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
We examined whether natural language processing and acoustic analysis of spoken biographical recall could identify lexical and temporal speech features associated with language and memory performance in TLE. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
A bstract In this study, we build EEG based graph model that uses frequency-resolved connectivity features, with Coherence, phase locking value (PLV) and phase lag index (PLI) in five frequency bands as multi-dimensional edge features. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
TAR DNA-binding protein 43 (TDP-43) is a key pathological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) and a critical regulator of RNA splicing. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The theta/alpha ratio is a promising but specification-dependent marker of cognitive impairment, contingent particularly on ICA and spectral power quantification. 4 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD) is a common cause of early-onset dementias marked by progressive declines in behavior, cognition, and/or movement. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Only the reliability half of that contrast is individually significant. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Structured Abstract INTRODUCTION Tau pathology typically occurs in Alzheimeŕs disease (AD), however is also frequently present in Parkinsońs disease dementia (PDD) and Dementia with Lewy Bodies (DLB), yet its disease-specific signature is unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid precursor protein (APP) is heavily studied as the source of amyloid beta in Alzheimer’s disease (AD), however, the complex functions of APP remain poorly understood, as does the impact of APP dosage on neurodevelopment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Adults with Down syndrome (DS) develop Alzheimer’s disease (AD) brain pathology by age 40 due to triplication of the Amyloid Precursor Protein ( APP ) gene on chromosome 21. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dysregulated expression and activity of DYRK1A, dual specificity tyrosine phosphorylation regulated kinase 1A, is a feature of several neurodevelopmental and neurodegenerative diseases, including Down syndrome, DYRK1A syndrome, autism spectrum disorders, Alzheimer’s disease, and Parkinson’s disease. 1 key finding →
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 →