INTRODUCTIONAlzheimers, Lewy body and vascular neuropathology underpin the most common forms of dementia. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Research
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cellular mechanisms in early Alzheimers disease (AD) remain poorly understood despite generation of extensive observational multiomic data. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The lipids and proteins that comprise lipid droplets regulate several cellular functions including lipid storage, stress responses, and inflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
To better characterize the genetic architecture underlying Alzheimer's disease (AD) and related dementia (ADRD), we performed a meta-analysis of European ancestry genome-wide association studies in 128,681 cases or proxy cases of ADRD and 849,833 (proxy) controls. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Established AD risk factors, including APOE ε4 dosage and polygenic risk scores, were not associated with disease progression amyloid positive individuals who are actively declining. 5 key findings →
Design: meta-analysis Participants: 222 Evidence: high
Full summary, score breakdown and related studies → Original source
Almost every recent Alzheimer's disease (AD) genome-wide association study (GWAS) has performed meta-analysis to combine studies with clinical diagnosis of AD with studies that use proxy phenotypes based on parental disease history. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The cross-ancestry Bayesian PRS model demonstrated the highest predictive performance in non-European populations. 3 key findings →
Evidence: moderate
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
The choroid plexus (CP) regulates barrier integrity, cerebrospinal-fluid (CSF) dynamics, and immune surveillance, yet its role in Alzheimer's disease (AD) remains poorly defined. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single cell RNA sequencing has opened a window into clarifying the complex underpinnings of disease, particularly in quantifying the relevance of tissue- and cell-type-specific gene expression. 1 key finding →
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
Spatial biology technologies enable high-dimensional profiling within intact tissues, revealing how molecular and cellular organization drives function and disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
16/100
The complexity of Alzheimer's disease (AD) manifests in diverse clinical phenotypes, including cognitive impairment and neuropsychiatric symptoms (NPSs). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single-nucleus transcriptomic studies have revealed glial cell states associated with Alzheimer's disease; however, these nuclei are dissociated from the complex architecture of the human neocortex. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
16/100
Alzheimer's disease (AD) is the most common neurodegenerative disorder, yet the molecular mechanisms underlying its region- and cell-type-specific pathogenesis remain poorly defined. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Triggering Receptors Expressed on Myeloid cells (TREMs) are a family of cell-surface receptors instrumental in the activation of different myeloid cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The full cohort included 1044 participants, of whom 779 comprised the proteomics cohort. 5 key findings →
Design: longitudinal study Participants: 674 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Psychosis is a neuropsychiatric feature found across neurodegenerative conditions including Alzheimer’s disease (AD) and Parkinson’s disease (PD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) develops over decades, but biological processes underlying susceptibility during midlife remain poorly understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Across all cases, the SNCA association was indexed by a 5′ signal previously associated with dementia with Lewy bodies and rapid eye movement sleep behaviour disorder, rather than the canonical 3′ Parkinson’s disease variant. 4 key findings →
Design: meta-analysis Participants: 1,362 Evidence: high
Full summary, score breakdown and related studies → Original source
How amyloid-β (Aβ) plaques and tau phosphorylation spatially relate to cell response and genetic variation in Alzheimer’s disease (AD) brain is currently unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study represents the largest PD AAO meta-analysis in European-ancestry populations to date. 5 key findings →
Design: meta-analysis Participants: 50,859 Evidence: high
Full summary, score breakdown and related studies → Original source
In the primary matched-feature comparison, reference areas under the receiver operating characteristic curve (AUCs) were 0.851 for ADNI tau90, 0.860 for ADNI tau180, and 0.933 for OASIS3 tau180. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease (AD) affects women more than men, with risk increasing during and after the menopausal transition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Large-scale genetic and preclinical studies strongly implicate myeloid cells, particularly brain-resident macrophages, in the pathogenesis of Alzheimer’s disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 29,380 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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 →