Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Symptomatic DIAD participants who had been treated for ∼ 4 years with anti-Aβ monoclonal antibodies (gantenerumab, n=4 or solanezumab, n=4) were compared with untreated, symptomatic DIAD mutation carriers (n=40) and with age-relevant non-DIAD controls with modest or no plaque pathology (n=18). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
GWAS found associations between plasma biomarkers and the APOE gene. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Phase 1 (realist review; 86 papers) identified that a key intervention component was the activities enabling the development of moments of connection. 1 key finding →
Design: randomized controlled trial Participants: 32 Evidence: high
Full summary, score breakdown and related studies → Original source
An extra copy of the amyloid precursor protein gene (APP) is present in Down syndrome (DS) and APP duplication (APPdup), increasing the risk of Alzheimer disease (AD) and cerebral amyloid angiopathy (CAA). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent clinical and epidemiological studies support the contention that diabetes mellitus (DM) is a strong risk factor for the development of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease,* the most common cause of dementia, affects an estimated 6.5 million persons aged ≥65 years in the United States (1). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic pain (i.e., pain lasting ≥3 months) is a debilitating condition that affects daily work and life activities for many adults in the United States and has been linked with depression (1), Alzheimer disease and related dementias (2), higher suicide risk (3), and substance use and misuse (4). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Artificial intelligence can assist providers in a variety of patient care and intelligent health systems. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
At baseline, higher AgeAccelPheno was associated with lower amyloid-β42 to amyloid-β40 (Aβ42:Aβ40) ratio, and higher AgeAccelGrim2 was associated with elevated neurofilament light (NfL). 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
16/100
Blood-based biomarkers have expanded access to biologically supported diagnosis of Alzheimer's disease (AD), particularly through measurement of amyloid-beta (Aβ) and phosphorylated tau species1-3. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aβ42/40 and Aβ37/42 ratios were associated with AAO across PSEN2 variants, strongly driven by PSEN2 variants with PSEN1 homologs. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) is a major risk factor for neurodegenerative diseases, including Alzheimer's disease (AD), yet the mechanistic link remains unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Biological aging is the correlated decline of multi-organ system integrity central to the etiology of many age-related diseases. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Epigenetic clocks can predict pathological aging associated with Alzheimer's disease (AD) risk, albeit findings are mixed regarding if clocks are predictive in blood and in non-European populations. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
While hippocampal (H) and inferior parietal lobule (IPL) atrophy are used routinely in Alzheimer's disease (AD) diagnostics, the role of enlarged choroid plexus (ChP) remains unclear. 2 key findings →
Participants: 872 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic work-up of dementia in clinical practice and the design of clinical trials. 4 key findings →
Design: longitudinal study Participants: 426 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results demonstrate that the multi-modal classifier achieved strong classification performance (accuracy = 68.64%; precision = 73.97%; F1-score=74.48%), with the highest recall (76.39%) from a model incorporating demographics and driving features, and prediction performance (accuracy = 70.48%; precision = 71.88%; F1-score = 74.80%, recall = 77.97%). 1 key finding →
Participants: 118 Evidence: low
Full summary, score breakdown and related studies → Original source
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
16/100
Trem2*R47H mice had alternative splicing leading to reduced Trem2 expression; Trem2*R47HHSS mice expressed Trem2 at wild-type transcript and protein levels. 4 key findings →
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 27,780 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.
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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →