27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Effective, scalable dementia prevention interventions are needed to address modifiable risk factors given global burden of dementia and challenges in developing disease-modifying treatments. 1 key finding →
Design: randomized controlled trial Participants: 6,104 Evidence: high
Full summary, score breakdown and related studies → Original source
Understanding the lifetime risk of dementia can inform public health planning and improve patient engagement in prevention. 1 key finding →
Design: cohort Participants: 15,043 Evidence: high
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Dominantly inherited Alzheimer's disease (DIAD) causes predictable biological changes decades before the onset of clinical symptoms, enabling testing of interventions in the asymptomatic and symptomatic stages to delay or slow disease progression. 2 key findings →
Evidence: high
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Dementia is a leading cause of death and disability worldwide. 3 key findings →
Design: RCT Participants: 33,995 Evidence: high
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An unresolved question for the understanding of Alzheimer's disease (AD) pathophysiology is why a significant percentage of amyloid-β (Aβ)-positive cognitively unimpaired (CU) individuals do not develop detectable downstream tau pathology and, consequently, clinical deterioration. 5 key findings →
Design: cohort Participants: 1,016 Evidence: moderate
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Clonal hematopoiesis of indeterminate potential (CHIP) is a premalignant expansion of mutated hematopoietic stem cells. 5 key findings →
Design: meta-analysis Participants: 1,362 Evidence: high
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Liraglutide, a glucagon-like peptide 1 (GLP-1) agonist and antidiabetic drug, has shown neuroprotective effects in animal models. 3 key findings →
Design: phase-2-trial Participants: 204 Evidence: null result
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Rates of cognitive decline in Alzheimer's disease (AD) are extremely heterogeneous. 1 key finding →
Design: case-control study Participants: 3,397 Evidence: moderate
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Compelling experimental evidence suggests that microglial activation is involved in the spread of tau tangles over the neocortex in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 130 Evidence: moderate
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p75 neurotrophin receptor (p75 NTR ) signaling pathways substantially overlap with degenerative networks active in Alzheimer disease (AD). 2 key findings →
Participants: 242 Evidence: high
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A major unanswered question in the dementia field is whether cognitively unimpaired individuals who harbor both Alzheimer's disease neuropathological hallmarks (that is, amyloid-β plaques and tau neurofibrillary tangles) can preserve their cognition over time or are destined to decline. 3 key findings →
Participants: 1,325 Evidence: low
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Plasma phosphorylated tau181 (P-tau181) might be increased in Alzheimer's disease (AD), but its usefulness for differential diagnosis and prognosis is unclear. 2 key findings →
Participants: 589 Evidence: moderate
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Citalopram is effective in treating agitation in Alzheimer's dementia (AD), but it is associated with cognitive and cardiac risks, likely due to its R-enantiomer. 5 key findings →
Design: phase-3-trial Participants: 173 Evidence: null result
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Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. 2 key findings →
Design: cross-sectional Participants: 187 Evidence: moderate
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With the emergence of Alzheimer's disease (AD) disease-modifying therapies, identifying patients who could benefit from these treatments becomes critical. 1 key finding →
Participants: 1,422 Evidence: moderate
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Triggering receptor expressed on myeloid cells 2 (TREM2) regulates microglial function and is implicated in Alzheimer's disease (AD) pathogenesis. 2 key findings →
Design: phase-2-trial Participants: 381 Evidence: null result
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African heritage diets are increasingly being replaced by Western-style dietary patterns because of urbanization, economic development, increased access to processed foods, globalization and changing social norms. 2 key findings →
Design: randomized controlled trial Evidence: high
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Tau plays a key role in Alzheimer's disease (AD) pathophysiology, and accumulating evidence suggests that lowering tau may reduce this pathology. 1 key finding →
Design: phase-1-trial Participants: 46 Evidence: early
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Differential diagnosis of dementia remains a challenge in neurology due to symptom overlap across etiologies, yet it is crucial for formulating early, personalized management strategies. 1 key finding →
Participants: 51,269 Evidence: low
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A combination of plasma phospho-tau (P-tau) and other accessible biomarkers might provide accurate prediction about the risk of developing Alzheimer's disease (AD) dementia. 2 key findings →
Participants: 340 Evidence: low
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GRN mutations cause progranulin haploinsufficiency, which eventually leads to frontotemporal dementia (FTD-GRN). 4 key findings →
Design: clinical trial Evidence: moderate
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Alzheimer's disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. 2 key findings →
Design: longitudinal study Participants: 1,612 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Predicting not just if, but also when, cognitively unimpaired individuals are likely to develop onset of Alzheimer's disease (AD) symptoms would be useful to clinical trials and, eventually, clinical practice. 2 key findings →
Design: cohort Participants: 603 Evidence: moderate
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Risk stratification is critical for the early identification of high-risk individuals and disease prevention. 3 key findings →
Participants: 117,981 Evidence: low
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Brain clocks, which quantify discrepancies between brain age and chronological age, hold promise for understanding brain health and disease. 4 key findings →
Participants: 5,306 Evidence: low
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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 →