27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
While single-cell measurements of the Alzheimer’s disease (AD) brain allow investigation of vulnerable cells in unprecedented depth, reported findings are heterogeneous, mostly descriptive and often ignore interdependence of cellular responses. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Transcriptomic and proteomic studies have consistently demonstrated substantial molecular heterogeneity across patients with Alzheimer’s disease (AD) and other neurodegenerative disorders, leading to the proposal of multiple disease subtypes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a widely prevalent neurodegenerative disorder characterized by progressive cognitive impairment and neuropathological alterations. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Individuals with comparable Alzheimer’s disease (AD) pathology can differ markedly in cognition, but the molecular nature of this heterogeneity remains unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synapse loss is the strongest pathological correlate of cognitive decline in Alzheimer’s disease, yet the molecular basis of synaptic vulnerability across disease progression remains poorly understood. 2 key findings →
Participants: 67 Evidence: low
Full summary, score breakdown and related studies → Original source
MicroRNAs (miRNAs) are implicated in Alzheimer's disease (AD), but research has focused on individual miRNAs and direct targets. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the deposition of amyloid-beta (Aβ) and microtubule-associated protein tau (MAPT) neurofibrillary tangles in the brain; however, the molecular mechanisms underlying associated synaptic dysfunction remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Auditory dysfunction can precede clinical dementia, but the molecular progression of Alzheimer disease (AD) pathology from the sensory periphery to auditory cortex remains poorly resolved. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings demonstrate that Tau deletion induces an active, multilevel gain-of-resilience rather than passive resistance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Whether the nodal vulnerability in dementia is solely represented by changes in cellular abundance or attrition of cellular transcriptomic landscape attribute to that transition in aging brain is yet to uncover with minutiae. 5 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
The retina displayed earlier and broader AD-related molecular alterations than the hippocampus. 4 key findings →
Evidence: low
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
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
Formalin-fixed, paraffin-embedded (FFPE) brain tissue is a major archival resource, yet its suitability for high-density DNA methylation profiling is limited by fixation-induced DNA fragmentation and crosslinking. 4 key findings →
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
Frontotemporal dementia (FTD) caused by progranulin (GRN) mutations is associated with pronounced thalamic degeneration, yet the cellular basis of selective thalamic vulnerability remains poorly understood. 3 key findings →
Participants: 92 Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS), caused by trisomy 21, confers a near-universal risk for Alzheimer’s disease (AD), yet individuals exhibit marked variability in cognitive decline, suggesting the presence of cellular mechanisms that modulate vulnerability and resilience. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid plaques contain numerous proteins in addition to amyloid beta in Alzheimer’s disease (AD). 4 key findings →
Participants: 240 Evidence: low
Full summary, score breakdown and related studies → Original source
MicroRNA dysregulation is implicated in neurodegenerative disorders, including Alzheimer’s disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The integrated stress response (ISR) is a highly conserved network essential for maintaining cellular homeostasis and cognitive function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging muscle showed increased inflammatory, extracellular-matrix, and stromal communication programs. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DNA cytosine modifications play a crucial role in gene regulation that underlies the pathogenesis of complex diseases such as Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
8 of the 274 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 8. The same 8 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 →