Regional binding of 3 H-THK5117 and 3 H-THK5351 was similar, except in the temporal cortex, which showed higher 3 H-THK5117 binding. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Regional binding of 3 H-THK5117 and 3 H-THK5351 was similar, except in the temporal cortex, which showed higher 3 H-THK5117 binding. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The aim of this study was to explore the relationship between cerebrospinal fluid Alzheimer's disease (AD) markers and depression in elderly people. 4 key findings →
Participants: 183 Evidence: low
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Cognitively normal participants (mean age 57.6 years) from the Gipuzkoa Alzheimer Project study were classified as having high risk (HR; n = 82) or low risk (LR; n = 293) for dementia according to a CAIDE score cutoff of 9. 4 key findings →
Participants: 82 Evidence: low
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Lewy body patients showed a significantly higher degree of WMSA in the external capsule cholinergic pathway despite no significant differences in global WMSA compared to controls. 4 key findings →
Participants: 82 Evidence: moderate
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The findings provide further in vivo evidence that astrocytosis occurs early in AD, preceding Aβ plaque deposition. 5 key findings →
Evidence: low
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The [(11)C]PIB uptake of the patients with AD did not increase significantly during follow-up when compared with that of the controls. 2 key findings →
Evidence: low
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Alzheimer's disease (AD) remains a clinical diagnosis but biomarkers from cerebrospinal fluid (CSF) and more lately amyloid imaging with positron emission tomography (PET), are important to support a diagnosis of AD. 4 key findings →
Participants: 64 Evidence: low
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The global prevalence of dementia is increasing. 1 key finding →
Evidence: low
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Epidemiological studies consistently indicate a two- to threefold increased risk of dementia among individuals with schizophrenia, although estimates vary due to diagnostic and ascertainment biases. 5 key findings →
Design: longitudinal study Evidence: moderate
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These results suggest that neuronal injury markers such as VLP-1 may have utility as biomarkers for AD. 5 key findings →
Evidence: low
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Object The authors describe the first clinical trial with encapsulated cell biodelivery (ECB) implants that deliver nerve growth factor (NGF) to the cholinergic basal forebrain with the intention of halting the degeneration of cholinergic neurons and the associated cognitive decline in patients with Alzheimer disease (AD). 1 key finding →
Design: open-label trial Evidence: moderate
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Grey matter changes in PDD involve areas associated with Alzheimer-like pathology while fronto-parietal abnormalities are possibly an early marker of PD cognitive decline. 4 key findings →
Evidence: low
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The AddNeuroMed and ADNI cohorts were combined giving a total of 329 healthy controls, 421 mild cognitive impairment patients, and 286 Alzheimer's disease (AD) patients. 4 key findings →
Participants: 329 Evidence: low
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Astrocytosis shows a distinct regional pattern in AD brain compared to fibrillar Aβ, suggesting that different types of astrocytes may be associated with the pathophysiological processes in AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The clusters of significant depression and compensation were further used as volumetric regions of interest (ROIs) in a brain interregional correlation analysis in each prodromal AD subgroup to explore metabolic connectivity. 3 key findings →
Evidence: low
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γ-Secretase modulators (GSMs) represent an emerging oral therapy for preventing and targeting Aβ-amyloidosis in Alzheimer disease. 3 key findings →
Evidence: low
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Hyperphosphorylated tau protein deposits and, inflammatory processes are characteristic components of Alzheimer disease (AD) pathology. 5 key findings →
Evidence: low
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Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions. 5 key findings →
Evidence: low
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In a previous study, we found that human neural stem cells (HNSCs) exposed to high concentrations of secreted amyloid-precursor protein (sAPP) in vitro differentiated into mainly astrocytes, suggesting that pathological alterations in APP processing during neurodegenerative conditions such as Alzheimer's disease (AD) may prevent neuronal differentiation of HNSCs. 5 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
Aβ is the main component of amyloid deposits in Alzheimer disease (AD) and its aggregation into oligomers, protofibrils and fibrils is considered a seminal event in the pathogenesis of AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Copy number variation (CNV) of the amyloid-β precursor protein gene (APP) is a known cause of autosomal dominant Alzheimer disease (ADAD), but de novo genetic variants causing ADAD are rare. 2 key findings →
Evidence: low
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Reimbursement decisions for new Alzheimer's disease (AD) treatments are informed by economic evaluations. 3 key findings →
Evidence: moderate
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Higher total meat consumption (red meat: 51%, poultry: 20%, processed meat: 29%), was associated with a better cognitive trajectory only in the APOE34/44 stratum (β per 1 z-unit increase: 0.011; CI: 0.004 to 0.018 versus -0.003; CI: -0.008 to 0.003; P for interaction = 0.002). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In vivo 11 C-PBB3 binding to the rTg4510 neocortex/hippocampus was increased relative to controls and correlated with local atrophy. 5 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 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 →