29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Haploinsufficiency of progranulin (resulting from mutations in the GRN gene) is a major genetic cause of frontotemporal dementia (FTD), which is characterized by profound changes in personality and behavior, progressive impairments in executive function, speech, language and/or movement, TDP-43 pathology, lysosomal dysfunction, and neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings shift AD modeling from passive proteotoxicity to an active, misregulated developmental structural engine, offering a mechanical framework that explains early olfactory vulnerability and non-linear anti-tau clinical trial responses. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Long non-coding RNAs (lncRNAs) are increasingly recognized as regulators of brain cell function, but their roles in astrocyte biology and neurodegeneration remain poorly understood. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aberrant alternative splicing alters multiple disease-associated splicing events, including MAPT exon 10 inclusion linked to tau pathology, and thereby impacts Alzheimer’s disease (AD) progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulation of tau tangles and Aβ plaques are prominent neuropathologies that characterize Alzheimer’s disease (AD) and Down Syndrome (DS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and Down Syndrome (DS) are characterized by the aggregation of tau tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer’s disease (AD) and related tauopathies, progressive pathology has been linked to prion mechanisms whereby ordered tau assemblies, or “seeds,” form in one cell and transit to neighboring or connected cells where they serve as templates for their own replication. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current Alzheimer’s disease (AD) immunotherapeutics face efficacy and safety limitations with antibody-based approaches. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondrial dysfunction, oxidative stress, neuroinflammation, and impaired protein homeostasis form interconnected pathological networks in acute central nervous system injury and chronic neurodegenerative disease. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease is increasingly linked to metabolic dysfunction, with insulin resistance emerging as a key contributor to tau pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Scrapie, a prion disease, is usually considered a protein-only infection. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings implicate significant liver–brain crosstalk through which chronic alcohol exposure may modulate AD-relevant pathology and reinforce the growing recognition of the liver as a critical organ in AD pathogenesis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) are central regulators of synaptic homeostasis, plasticity, and dysfunction during Alzheimer’s disease (AD) progression. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder for which effective multitarget therapies remain unavailable. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
IKZF1 is prioritised as a candidate late-disease microglial TF, supported by six convergent evidence dimensions including independent bulk replication. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Lipid-processing microglia are among the microglial states most strongly associated with Alzheimer’s disease (AD) pathology, yet whether this association reproduces across independent cohorts, what transcriptional programs define the state, and which upstream signals and small molecules can modulate it remain unsolved. 3 key findings →
Participants: 150 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 2711 decedents (mean [SD] age, 73.4 [14.4] years; range, 23 to 111 years; 1340 [49.4%] female), 531 (19.6%) met both thresholds, 270 (10.0%) the amyloid threshold only, 207 (7.6%) the tau threshold only, and 1703 (62.8%) neither. 3 key findings →
Design: cross-sectional Participants: 1,467 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Biological definitions of neuronal α-synuclein disease are advancing diagnosis beyond traditional clinical syndromes, but the trajectories preceding dementia and the influence of concomitant Alzheimer pathology remain uncertain. 3 key findings →
Design: longitudinal study Participants: 1,543 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Many biological quantities in omics are inherently periodic or directional, including circadian phase, cell-cycle position, and cellular orientation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sleep disturbance in Alzheimer’s disease (AD), particularly the reduction of slow wave sleep (SWS), has been proposed as a novel therapeutic target, with disease-modifying potential. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is characterised by progressive accumulation of misfolded proteins and failure of cellular clearance pathways, particularly the autophagy–lysosomal system. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Our findings indicate that HFOs likely arise from different neuronal populations and are generated through distinct mechanisms in these two models. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injuries (TBIs) are associated with increased risk of neurodegenerative disease, including Alzheimer’s disease (AD); however, the mechanisms by which TBI promotes AD pathogenesis remain poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 8,203 studies in this tag that have a study page, 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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →