27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Although Alzheimer’s disease (AD) and glioblastoma (GBM) share common aging-related risk factors, they lead to opposite cellular fates—neurodegeneration versus uncontrolled proliferation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single-nucleus RNA-seq (snRNA-seq) studies of Alzheimer’s disease (AD) routinely filter nuclei by mitochondrial percentage (%MT) or remove mitochondrial genes, yet whether these reads carry information about cognition is rarely examined. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For a long time, the protein coding potential of our genome was underestimated. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Computational drug repurposing commonly relies on transcriptomic signature matching to identify compounds that reverse disease-associated gene expression, but such approaches do not distinguish putative causal drivers from downstream consequences of disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a progressive, neurodegenerative disorder and the leading cause of dementia worldwide. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In spatial proteomics across large cohorts, downstream estimates from tens of thousands of images depend on accurate cell segmentation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study investigated volumetric MRI differences of the thalamic nuclei in asymptomatic young adult C9orf72 expansion carriers compared to non-carriers, and examined spatial associations with normative thalamic transcriptomics from 8 weeks post-conception through middle age. 3 key findings →
Participants: 72 Evidence: low
Full summary, score breakdown and related studies → Original source
We then integrated healthy retinal expression, AD retinal proteomics, and PD aqueous-humor proteomics with the brain-concordance results. 3 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
Capturing the systemic effects of drugs in vivo remains a fundamental challenge for drug repurposing strategies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Severe cognitive decline due to dementia is an important clinical indicator signaling neurodegeneration. 5 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
Neurodegenerative diseases are a major threat to older adults and represent a growing global health burden as the elderly population continues to expand. 1 key finding →
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
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
Postmitotic neurons must preserve genome integrity for decades despite continuous oxidative, transcription-associated, and environmental DNA damage. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Late-life depression (LLD) is increasingly recognized as a complex multisystem disorder associated with accelerated biological aging, impaired physiological resilience, frailty, and an increased risk of cognitive decline and dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings identify restoration of hippocampal transcript fate and splice-isoform selection as a mechanism potentially underlying A. muciniphila -mediated protection against Cd neurotoxicity, and establish post-transcriptional RNA regulation as a gut-brain target for mitigating environmentally driven neurotoxicity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) staging based on amyloid-β, tau, and neurodegeneration does not capture heterogeneous microglial functions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, in which epitranscriptomic modifications, especially RNA methylation, may exert crucial regulatory effects. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ORIGIN-PD enables rational enrichment for NLRP3/NF-κB inhibitor trials by identifying patients with inflammatory involvement. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Amaryllidaceae geophyte Lycoris radiata is a primary botanical source of high-value medicinal alkaloids, including the Alzheimer’s therapeutic galanthamine. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 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 9. The same 9 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 →