28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Aβ(+) patients with TES (N = 10), but not Aβ(-) TES, had significantly higher plasma P-tau levels than HC (P-tau181: p d = 1.34; P-tau217: p d = 1.59). 3 key findings →
Participants: 18 Evidence: low
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Within a heterogenous group of MCI patients, including many with clinically significant CVD, baseline memory and executive performance significantly predicted likelihood to develop dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Low CSF Abeta(1-42) (surrogate for Abeta amyloid load) is more closely linked to the presence of APOE epsilon4 than to clinical status. 3 key findings →
Participants: 399 Evidence: low
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Sex or gender differences in the risk of Alzheimer's disease and related dementias (ADRD) differ by world region, suggesting that there are potentially modifiable risk factors for intervention. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Clinical and neuropsychological features contribute to delineating the spectrum of pathology underlying a patient diagnosed with FTLD, but biomarkers are needed that, together with the clinical phenotype, can predict the underlying neuropathology. 5 key findings →
Evidence: low
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Most patients with svMCI do not exhibit substantial amyloid burden, and CVD does not increase β-amyloid burden as measured by amyloid imaging. 5 key findings →
Design: cross-sectional Participants: 95 Evidence: low
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Hippocampal sclerosis (HS) is a common and often asymmetric neuropathological finding among elderly persons who experience progressive memory loss, but its cause is unknown and it is rarely diagnosed during life. 1 key finding →
Design: longitudinal study Evidence: moderate
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TAR DNA-binding protein 43 (TDP-43) aggregation is the most common pathological hallmark in frontotemporal dementia (FTD) and characterizes nearly all patients with motor neuron disease (MND). 3 key findings →
Participants: 17 Evidence: low
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Overall, 92% of patients had one or more dementia-related behaviors. 3 key findings →
Design: cross-sectional Participants: 5,776 Evidence: low
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No large-scale characterizations of neurofilament light chain (NfL) have been conducted in diverse populations. 1 key finding →
Participants: 890 Evidence: low
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Although air pollution is well known to be harmful to the lung and airways, it can also damage most other organ systems of the body. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As a result, our combined method achieved an area under the receiver operating characteristic (AU-ROC) curve of 98.33, 93.59, 96.83, 94.64, 96.43, and 95.24% for AD vs. MCIs subjects which are high relative to single modality results and other state-of-the-art approaches. 2 key findings →
Participants: 158 Evidence: low
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These findings suggest that the sleep-wake cycle plays a crucial part in brain ageing, pointing to a potential avenue for improvement of cognitive outcomes in people at risk of cognitive decline and dementia. 1 key finding →
Evidence: low
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We believe this information important when counseling elderly patients regarding the risks of mortality and PJI after TKA and risk-adjusting publicly reported TKA patient outcomes. 2 key findings →
Participants: 83,011 Evidence: low
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Patients with isolated rapid-eye-movement sleep behaviour disorder (RBD) are commonly regarded as being in the early stages of a progressive neurodegenerative disease involving α-synuclein pathology, such as Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy. 1 key finding →
Evidence: low
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Defects in DNA repair have been extensively linked to neurodegenerative diseases, but the exact mechanisms remain poorly understood. 3 key findings →
Evidence: low
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ADNI-3 will aim to inform AD treatment trials and facilitate development of AD disease-modifying treatments. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) results in cognitive decline and altered network activity, but the mechanisms are unknown. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Abnormal accumulation of the amyloid-beta peptide (Abeta) in the brain appears crucial to pathogenesis in all forms of Alzheimer disease (AD), but the underlying mechanisms in the sporadic forms of AD remain unknown. 4 key findings →
Evidence: low
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White matter alterations are present in the majority of patients with Alzheimer's disease type dementia. 4 key findings →
Evidence: low
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Depression is a known risk factor for dementia and MCI, but its associations with AT(N) biomarkers remain inconsistent and may differ by cognitive status. 4 key findings →
Design: longitudinal study Participants: 2,929 Evidence: moderate
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There is a paucity of longitudinal research investigating the relations between atrial fibrillation (AF) and domain-specific cognitive performance. 4 key findings →
Design: cross-sectional Participants: 2,682 Evidence: moderate
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AD exhibited elevated serum GFAP levels in comparison to control patients (P < 0.0001). 5 key findings →
Participants: 1,273 Evidence: moderate
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Among 24 762 people with HIV and 494 963 people without HIV (86.9% men, 45.5% White, 23.1% Black, 20.3% Hispanic), incident dementia diagnoses declined from 2000 to 2023 in both people with and without HIV (-7.68 and -2.70% per period, respectively). 5 key findings →
Design: retrospective cohort Participants: 762 Evidence: moderate
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Early detection of Alzheimer's disease (AD) is critical yet challenging, particularly in younger individuals. 1 key finding →
Design: longitudinal study Participants: 120 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 →