28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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Concentrations of plasma p-tau181 were compared with established CSF and PET biomarkers and longitudinal measurements using Spearman correlation, area under the curve (AUC), and linear regression analyses. 1 key finding →
Design: longitudinal study Participants: 1,131 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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Whilst cerebrospinal fluid (CSF) and positron emission tomography (PET) biomarkers for amyloid-β (Aβ) and tau pathologies are accurate for the diagnosis of Alzheimer's disease (AD), their broad implementation in clinical and trial settings are restricted by high cost and limited accessibility. 3 key findings →
Design: longitudinal study Participants: 1,000 Evidence: moderate
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Plasma p-tau217 is a prognostic marker for identifying individuals who will develop cognitive impairment within ten years. 2 key findings →
Design: cohort Participants: 215 Evidence: moderate
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We analyzed 1,240 MRIs from 473 patients (age: 69.2 ± 7.4 [range: 49-87]; 32.8% women). 2 key findings →
Design: cohort study Participants: 1,240 Evidence: moderate
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The clinical diagnosis of probable AD dementia demonstrated good agreement with biologically defined AD (positive predictive value 85.2%). 3 key findings →
Design: cohort study Participants: 166 Evidence: moderate
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Among 641 participants with CSF Aβ42 data and at least two 18F-florbetapir scans, 335 (52.3%) were male. 4 key findings →
Design: cohort study Participants: 402 Evidence: moderate
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Data from 3960 MRI sessions among 1141 participants were included: 252 pathogenic variant carriers from DIAN (mean [SD] age, 38.4 [11.2] years; 137 [54%] female), 571 older adults from ADNI (mean [SD] age, 72.8 [7.3] years; 274 [48%] female), and 318 older adults from HABS (mean [SD] age, 72.4 [7.6] years; 194 [61%] female). 3 key findings →
Design: cohort study Participants: 1,141 Evidence: moderate
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Females are disproportionately affected by dementia due to Alzheimer's disease. 4 key findings →
Design: longitudinal study Participants: 457 Evidence: moderate
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Experimental evidence suggests that activated microglia induce astrocyte reactivity in neurodegenerative disorders, such as Alzheimer's disease (AD). 3 key findings →
Design: cohort Participants: 352 Evidence: moderate
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Among 580 participants (PREVENT-AD, 128; HABS, 153; AIBL, 48; Knight ADRC, 251), mean (SD) age ranged from 67 (5) to 76 (6) years across cohorts, with between 55% (137/251) and 74% (95/128) female participants. 2 key findings →
Design: cohort study Participants: 580 Evidence: moderate
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Blood-based biomarkers for Alzheimer's disease (AD) pathology have been investigated intensively as markers for AD-related neurodegeneration. 5 key findings →
Design: cohort study Participants: 158 Evidence: moderate
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Parkinson's disease has a long prodromal stage with various subclinical motor and non-motor manifestations; however, their evolution in the years before Parkinson's disease is diagnosed is unclear. 5 key findings →
Design: longitudinal study Evidence: moderate
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Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models. 5 key findings →
Design: longitudinal study Participants: 1,702 Evidence: moderate
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Common variants within TMEM106B are associated with risk for frontotemporal lobar degeneration with TDP-43 pathology (FTLD-TDP). 4 key findings →
Design: cohort study Participants: 518 Evidence: moderate
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A framework for multi-centre MRI studies of Alzheimer's disease has been established consisting of a harmonized MRI acquisition protocol across centres, rigorous QC at both the sites and central data analysis hub and an automated image analysis pipeline. 4 key findings →
Design: longitudinal study Participants: 378 Evidence: moderate
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Our results demonstrate that different MAPT mutations give rise to distinct atrophy patterns and clinical phenotype, providing insights into the underlying disease biology and potential utility for patient stratification in therapeutic trials. 3 key findings →
Design: cohort study Evidence: moderate
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Within the training set, individuals closer to or beyond their parent's symptom onset demonstrated reduced grey matter volume and altered functional connectivity, specifically in regions known to be vulnerable in Alzheimer's disease. 5 key findings →
Design: longitudinal study Participants: 138 Evidence: moderate
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White matter hyperintensities (WMHs) are commonly assumed to represent non-specific cerebrovascular disease comorbid to neurodegenerative processes, rather than playing a synergistic role. 4 key findings →
Design: longitudinal study Participants: 571 Evidence: moderate
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Chronic obesity is associated with several complications, including cognitive impairment and dementia. 4 key findings →
Design: cohort study Evidence: moderate
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(69.4% female) were aged 68.3 ± 5.1 years at their first PET scans. 5 key findings →
Design: longitudinal study Participants: 243 Evidence: moderate
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< 0.001). Stage-specific tau-PET region-of-interest selection reduced required sample sizes by 30%-93% for detecting hypothetical disease-modifying drug effects. 4 key findings →
Design: longitudinal study Evidence: moderate
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The study included 560 amyloid-positive participants (BioFINDER: n = 431; mean [SD] age, 73.6 [7.0] years; 212 female [49.2%] and 219 male [51.8%]; TRIAD: n = 129; mean [SD] age, 70.4 [8.3] years; 76 female [58.9%] and 53 male [41.1%]). 5 key findings →
Design: cohort study Participants: 431 Evidence: moderate
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These analyses suggest that CenTauR harmonization increases the comparability of tau‐PET data acquired with different tracers. 2 key findings →
Design: longitudinal study Participants: 1,089 Evidence: moderate
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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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →