27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyloid precursor protein (APP) mis-processing and aberrant tau hyperphosphorylation are causally related to the pathogenesis and neurodegenerative processes that characterize Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Plasma glial fibrillary acidic protein (GFAP) has emerged as a promising biomarker of astrocytic reactivity in preclinical Alzheimer´s Disease (AD). 4 key findings →
Participants: 143 Evidence: low
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Damaging nonsynonymous ABCA1 variants had differential AD risk effects between APOE genotype groups and exhibited interaction effects with APOE ε2 and ε4. 5 key findings →
Evidence: moderate
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These findings highlight normative modelling's utility in revealing the complex interplay among sex, age, and AD risk in shaping brain structure and cognition in later life. 5 key findings →
Design: longitudinal study Evidence: moderate
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= 0.71) longitudinally. YKL-40 associations with FW and FW-corrected fractional anisotropy were null. 4 key findings →
Design: cross-sectional Evidence: moderate
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For many years, blood-based biomarkers for Alzheimer's disease seemed unattainable, but recent results have shown that they could become a reality. 1 key finding →
Evidence: low
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Non-neurological surgery has both acute and long-term effects on the brain. 3 key findings →
Participants: 35 Evidence: low
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Plasma ptau217 has strong diagnostic performance in distinguishing CSF biomarker-defined AD in a clinically relevant, younger cohort of people with symptoms, adding further weight for a simple diagnostic blood test for AD as a cause of a patient's symptoms. 2 key findings →
Evidence: moderate
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Human stem cell models have the potential to provide platforms for phenotypic screens to identify candidate treatments and cellular pathways involved in the pathogenesis of neurodegenerative disorders. 1 key finding →
Evidence: low
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A population of >6 million people worldwide at high risk of Alzheimer’s disease (AD) are those with Down Syndrome (DS, caused by trisomy 21 (T21)), 70% of whom develop dementia during lifetime, caused by an extra copy of β-amyloid-(Aβ)-precursor-protein gene. 4 key findings →
Evidence: low
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Global PSP prevalence ranges between 5-6.4 per 100,000, influenced by diagnostic criteria and healthcare infrastructure. 5 key findings →
Evidence: low
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Dementia diagnosis relies on assessing functional decline, yet widely used assessment tools are often developed in Euro-American contexts, limiting their cross-cultural validity. 5 key findings →
Evidence: low
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The PIF for the total NZ population following a 15% risk factor reduction was 14.6% (95% confidence interval: 7.7-21.1) Modeled projections demonstrated prevalence reduction over time, from 1.0% at 10 years to 4.2% at 30 years. 5 key findings →
Evidence: low
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Recent Findings Recent observational data in adults with Down syndrome indicate that obstructive sleep apnoea is associated with adverse cardiometabolic, mortality and Alzheimer disease outcomes. 2 key findings →
Design: cohort study Evidence: moderate
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In UKB, higher 2-h post-load glucose was associated with a 69% increased Alzheimer's dementia risk (odds ratio 1.69 [95% confidence interval 1.38-2.07]), though this did not replicate in an independent GWAS. 5 key findings →
Participants: 357 Evidence: low
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We conclude that an inverse correlation between levels of inflammation in cortical areas and plasma NfL levels indicates that microglial activation may initially be protective to axons in AD. 3 key findings →
Evidence: low
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There was no significant difference between patients with dementia or depression in their wish to know their diagnosis. 4 key findings →
Evidence: low
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Only a minority of people with dementia receive a formal diagnosis despite a growing body of evidence highlighting the benefits of early diagnosis and intervention. 1 key finding →
Evidence: low
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Patients with advanced Parkinson's disease had a significantly higher disease impairment, longer disease duration, and an unstable motor response to levodopa with frequent on-off fluctuations. 5 key findings →
Participants: 29 Evidence: low
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Recent published clinical trial safety data showed that 41% of Alzheimer patients experienced amyloid-related imaging abnormalities (ARIA), marks of microhemorrhages and edema in the brain, following administration of Biogen's Aduhelm/aducanumab (amino acids 3-7 of the Aβ peptide). 4 key findings →
Evidence: low
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Dementia of Alzheimer Type (DAT) is increasingly detected at an earlier stage of the disorder, when interventions to assist with everyday memory difficulties might be most valuable. 4 key findings →
Evidence: low
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Neighborhood disadvantage is associated with education, health behaviors and mortality. 5 key findings →
Participants: 1,479 Evidence: moderate
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We found 5 distinct clusters of subjects (N=38, N=16, N=24, N=14, N=21) with a composition statistically independent from that obtained using available clinical diagnostic criteria (each cluster included all phenotypical groups). 3 key findings →
Participants: 20 Evidence: moderate
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The genetic architecture of sporadic Early-Onset Alzheimer Disease (sEOAD, onset ≤65 years) remains largely unknown. 2 key findings →
Evidence: low
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Amyloid-targeted monoclonal antibody therapies have introduced a new era in the treatment of early Alzheimer disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 27,780 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 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 →