27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Previous studies of Aβ plasma as a biomarker for Alzheimer's disease (AD) obtained conflicting results. 5 key findings →
Design: longitudinal study Participants: 715 Evidence: moderate
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One hundred eighty-seven participants with brain autopsy (NPDx1: AD n = 85; other n = 102; mean age: 74.3 years, 38.5% female; interval blood collection-death [mean ± SD]: 2.8 ± 1.6 years) and 67 NC without brain autopsy (mean age: 66.5 years, 71.6% female) were included. pTau217, but not GFAP, levels increased stepwise with increasing Thal phases (β = 0.61; 95% CI [0.24-0.97] to β = 0.91 [0.55-1.27]) and Braak stages (β = 0.59; [0.16-1.01] to β = 0.74 [0.33-1.15]). 5 key findings →
Design: cohort study Participants: 85 Evidence: moderate
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Despite remarkable progress in the biomarker field in recent years, local validation of plasma biomarkers of Alzheimer’s disease (AD) and dementia is still lacking in Latin America. 5 key findings →
Design: cohort study Participants: 49 Evidence: moderate
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This study validated PrecivityAD2, a mass-spectrometry blood test made by C2N Diagnostics that combines two markers (%p-tau217 and the amyloid-beta 42/40 ratio) into a single 'Amyloid Probability Score 2.' 4 key findings →
Design: cross-sectional Participants: 583 Evidence: high
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Serum NfL concentration is increased in FAD prior to symptom onset and correlates with measures of disease stage and severity. 3 key findings →
Design: cross-sectional Participants: 48 Evidence: low
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The use of an amyloid clock enabled visualization and analysis of biomarker changes as a function of estimated years from symptom onset in sporadic AD. 1 key finding →
Design: cross-sectional Participants: 118 Evidence: moderate
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Subjective cognitive decline (SCD) is proposed as an indicator of transitional disease stage 2 in the Alzheimer's disease (AD) continuum. 2 key findings →
Design: longitudinal study Participants: 457 Evidence: moderate
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Among the plasma biomarkers, phosphorylated tau (p-tau) 217 exhibited the highest concordance rate with Aβ (2326 of 2571 [90.5%]) and tau (100 of 120 [83.3%]) PET. 4 key findings →
Design: cohort study Participants: 2,611 Evidence: moderate
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This study examined whether levels of blood biomarkers of amyloid (Aβ 42 /Aβ 40 ratio), tau (p-tau 181 ), neurodegeneration (NfL), and glial activation and neuroinflammation (glial fibrillary acidic protein [GFAP], YKL40, soluble triggering receptor expressed on myeloid cells 2 [sTREM2]) collected when participants were cognitively normal are associated with the time to onset of MCI. 5 key findings →
Design: longitudinal study Participants: 271 Evidence: moderate
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Greater neighborhood disadvantage was associated with elevated inflammatory and AD CSF biomarkers cross-sectionally and longitudinal increases in a nonspecific inflammatory blood biomarker. 5 key findings →
Design: longitudinal study Participants: 334 Evidence: moderate
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All synaptic biomarkers tested had a good discriminatory power to distinguish patients with AD abnormal CSF from those with non-AD disorders. 4 key findings →
Design: cross-sectional Participants: 81 Evidence: moderate
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Serum tHcy levels were significantly higher and serum folate and vitamin B12 levels were lower in patients with DAT and patients with histologically confirmed AD than in controls. 4 key findings →
Design: case-control study Participants: 164 Evidence: moderate
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The advent of proteomics offers an unprecedented opportunity to predict dementia onset. 1 key finding →
Participants: 52,645 Evidence: low
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These results suggest that WMH primarily affect the risk of progression when CSF measures of neurodegeneration or neuronal injury (as reflected by t-tau) are low. 5 key findings →
Design: longitudinal study Participants: 274 Evidence: moderate
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Baseline CSF levels of NGRN in patients with AD (median level, 2381 pg/mL [interquartile range, 1651-3416 pg/mL]) were higher than in cognitively normal participants (median level, 1712 pg/mL [interquartile range, 1206-2724 pg/mL]) (P = .04). 3 key findings →
Design: longitudinal study Participants: 163 Evidence: moderate
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The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →
Design: longitudinal study Participants: 2,609 Evidence: moderate
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Neurofilament light (NfL) is a marker of neuroaxonal injury, a prominent feature of Alzheimer's disease. 4 key findings →
Design: cross-sectional Participants: 1,149 Evidence: moderate
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Evidence regarding the clinical validity of blood biomarkers of Alzheimer's disease (AD) in the general population is limited. 3 key findings →
Evidence: moderate
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Plasma p-tau217/Aβ42 had high accuracy to detect AD, with comparable performance across race. 2 key findings →
Design: cross-sectional Participants: 1,135 Evidence: moderate
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The diagnostic performance of plasma biomarkers was poor (area under the curve [AUC] between 0·53 [95% CI 0·44-0·62] and 0·74 [0·66-0·82]) except for plasma NfL concentrations, which had an AUC of 0·88 (0·82-0·93) for the differentiation of the asymptomatic group versus the prodromal Alzheimer's disease group and 0·95 (0·92-0·98) for the asymptomatic group versus the Alzheimer's disease dementia group. 4 key findings →
Design: cross-sectional Participants: 282 Evidence: low
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Among cognitively normal participants with positive biomarkers, 34.4% developed cognitive impairment (Clinical Dementia Rating > 0) as compared to 8.4% of those with negative biomarkers. 2 key findings →
Design: longitudinal study Participants: 720 Evidence: moderate
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Higher levels of P-tau181 (HR = 1.32 [95% CI: 1.17-1.51]), NfL (HR = 1.19 [95% CI: 1.03-1.36]), and GFAP (HR = 1.36 [95% CI: 1.22-1.52]), and a lower Aβ42/Aβ40 ratio (HR = 0.80 [95% CI: 0.68-0.95]) were associated with an increased risk of progressing to clinically-diagnosed DAT. 2 key findings →
Design: longitudinal study Participants: 1,007 Evidence: moderate
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Mean (SD) follow-up was 4.8 (2.6) years. 3 key findings →
Design: cohort study Participants: 298 Evidence: moderate
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Importantly, they suggest that these associations might be explained by a decrease of amyloidosis and tau-pathology. 2 key findings →
Design: cross-sectional Participants: 512 Evidence: moderate
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Among the evaluated parameters, the only significant predictor of conversion to AD was non-Cp copper (hazard ratio = 1.23, 95% confidence interval = 1.03-1.47, p = 0.022); for each additional micromole per liter unit (μmol/l) of non-Cp copper, the hazard increased by ~20%. 2 key findings →
Design: meta-analysis Participants: 42 Evidence: high
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9 of the 829 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 →