29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The co-occurrence of both Alzheimer disease (AD) pathology and vascular brain injury (VBI) is very common, especially amongst the oldest of old. 2 key findings →
Evidence: low
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Generated MR images from florbetapir PET showed signal patterns that were visually similar to the real MR. The structural similarity index between real and generated MR was 0.91 ± 0.04. 5 key findings →
Evidence: low
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Flortaucipir uptake distinguished individuals with PCA and amnestic AD dementia early in the symptomatic course. 2 key findings →
Evidence: low
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There is considerable interest in designing therapeutic studies of individuals at risk of Alzheimer disease (AD) to prevent the onset of symptoms. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of the 1,193 CI patients, 860 (72.1%) were amyloid-positive. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Global CL quantification of Aβ PET scans is highly concordant with visual interpretation. 3 key findings →
Evidence: moderate
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We demonstrated a moderate positive correlation between PDGFRβ and both total Tau and phosphorylated Tau 181 in cognitively normal individuals. 4 key findings →
Design: cross-sectional Evidence: moderate
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With the introduction of the new causal amyloid targeting therapies, the role of biomarker-assisted diagnosis of Alzheimer disease (AD) has received a further boost. 5 key findings →
Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia, accounting for 60-70% of all cases [Hebert et al., 2003, 1]. 5 key findings →
Evidence: low
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The authors' findings suggest that the effectiveness of explicit-memory training in patients with MCI is associated with training-specific increases in activation and connectivity in a distributed neural system that includes areas involved in explicit memory. 3 key findings →
Evidence: low
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Previous MRI studies reported cortical iron accumulation in early-onset (EOAD) compared to late-onset (LOAD) Alzheimer disease patients. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Saturation and competition binding studies of (3)H-THK5117 in post-mortem AD brain tissue showed the presence of multiple binding sites. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Older adults who report more severe acute or chronic pain have smaller hippocampal volumes and lower levels of hippocampal N-acetylaspartate/creatine, a marker of neuronal integrity. 3 key findings →
Evidence: low
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The non-fluent/agrammatic variant of primary progressive aphasia (nfvPPA) and the behavioral variant frontotemporal dementia (bvFTD) are focal neurodegenerative disorders belonging to the FTD-spectrum clinical syndromes. 1 key finding →
Evidence: low
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The white matter FC decreased in late MCI and AD dementia patients compared to CN participants, and this decrease was correlated with cognitive measures. 5 key findings →
Evidence: low
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There is accumulating evidence suggesting that changes in brain perfusion are present long before the clinical symptoms of Alzheimer's disease (AD), perhaps even before amyloid-β accumulation or brain atrophy. 2 key findings →
Evidence: low
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Twenty-three patients with mild cognitive impairment (MCI), 12 dementia of Alzheimer's type (DAT), and 14 normal controls were studied following the ADNI2 protocol. 4 key findings →
Evidence: moderate
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The present study was aimed to investigate the relationships between thyroid stimulating hormone (TSH), freeT3 (fT3) and freeT4 (fT4) and brain glucose consumption as detectable by means of 2-deoxy-2-(F-18) fluoro-D-glucose (F-18 FDG) Positron Emission Tomography/Computed Tomography (PET/CT) in a selected population with Alzheimer disease (AD). 4 key findings →
Participants: 87 Evidence: low
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It accounts for a quarter of the elderly population and is associated with cognitive decline. 4 key findings →
Participants: 111 Evidence: low
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Alzheimer's disease (AD) is a frequently observed, irreversible brain function disorder among elderly individuals. 4 key findings →
Evidence: low
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We investigated the performance of FDG PET using an automated procedure for discrimination between Alzheimer's disease (AD) and controls, and studied the influence of demographic and technical factors. 4 key findings →
Evidence: low
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Mild Cognitive Impairment (MCI) is a transitional stage between normal aging and dementia and people with MCI are at high risk of progression to dementia. 4 key findings →
Evidence: low
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Fifty-three scans (31.74%) were rated amyloid-positive by all readers, while 62 scans (37.13%) were rated as amyloid-negative by all readers. 5 key findings →
Evidence: low
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Amyloid PET enables improved detection of amyloid-β plaques within the brain. 5 key findings →
Evidence: low
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Fourteen participants (21.5%) converted to MCI, and 24 (36.9%) were classified as Prog-1.Plasma biomarkers did not show consistent predictive performance across predefined endpoints (all p>0.05), although NfL demonstrated modest discrimination for MCI conversion (area under the curve [AUC] 0.686, p=0.008).Hippocampal volume demonstrated significant discriminative performance for MCI conversion (AUC 0.765, p=0.016) and Prog-1 (AUC 0.933, p<0.001).For Prog-2, hippocampal volume showed high discrimination (AUC 0.952, p<0.001).WMH grade also demonstrated significant discrimination for MCI conversion (AUC 0.835, p<0.001) and Prog-1 (AUC 0.857, p<0.001).Bootstrap analyses (1,000 iterations) tended to show higher AUC estimates for imaging markers compared with plasma biomarkers. 2 key findings →
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.
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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →