27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
CSF phospho-tau (p-tau(181)) levels have shown good diagnostic utility in differential diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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It has been increasingly recognized that the pathological progress of Alzheimer´s disease (AD) is connected to metabolic function and inflammation. 4 key findings →
Participants: 18 Evidence: low
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The measurement of CSF specimens from Netherlands Brain Bank showed that the levels of total tau and p-tau in CSF specimens of AD patients were significantly higher than those in CSF of patients with VD and non-dementia neurological disorders, and of age-matched non- 4 key findings →
Participants: 52 Evidence: low
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. The area under the receiver operating characteristic curve of plasma p -tau217 was 0.941. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the study scenario, adding plasma p -tau217 testing to SCE reduced diagnostic costs by $342/patient, through more efficient use of amyloid PET and CSF testing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To evaluate plasma p-tau217 ability to detect pre-symptomatic Alzheimer disease (AD) in ethnoracially diverse cognitively normal individuals. 1 key finding →
Evidence: low
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Die Frühphasen- & R1-Bilder korrelierten signifikant in allen Gruppen (Gesunde: r=0,68-0,84; AD: r=0,81-0,9; PSP-RS: r=0,81-0,86; FTD: r=0,76-0,82). 5 key findings →
Participants: 26 Evidence: low
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We found that induction of adult human brain-like 4R Tau isoform expression enables endogenous formation of late-stage Tauopathy hallmarks in iPSC-derived neurons engineered to contain synergistic Tau mutations. 5 key findings →
Evidence: low
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The basal nucleus showed significant neuronal loss in PPA versus controls (p <0.05). 5 key findings →
Evidence: low
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PPA/3R had a mean age of 63.5 years (SD = 3.9), PPA/4R were 72.5 years (SD = 5.8), and controls were 63.4 years (SD = 6.8). 5 key findings →
Evidence: low
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PPA/3R had a mean age of 63.5 years (SD = 3.9), PPA/4R were 72.5 years (SD = 5.8), and controls were 63.4 years (SD = 6.8). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To the Editor: We have recently highlighted the potential pitfalls of amyloid-beta (Aβ) PET, suggesting that both Aβ and tau assessments are necessary to relate clinical symptoms to Alzheimer disease (AD) pathology.1 Herein, we would like to present 3 additional cases related to the clinical practice of disease-modifying therapy (DMT) for AD. 4 key findings →
Design: clinical trial Evidence: low
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Sowohl in der Tau- als auch in der Amyloid-PET-Bildgebung zeigte die Quantifizierung eine gute bis exzellente Vorhersage der visuellen Beurteilung (Tau: AUC=0,86, p<0,0001; Amyloid: AUC=0,99, p<0,0001). 5 key findings →
Participants: 201 Evidence: low
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Within around 700 new designed PROTACs, we found by computational modelling more than 25 PROTACs that were predicted to have a better ability to form ternary complexes than the previously reported PROTACs. 5 key findings →
Evidence: low
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We recently confirmed and extended these findings using recombinant TauOs generated from full-length human tau in the presence of arachidonic acid (Balducci et al., 2025; Figure 1). 5 key findings →
Evidence: low
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Semantic dementia (SD) is a type of dementia characterized by a loss of semantic memory, typically presenting with left-predominant temporal lobe atrophy and a frontotemporal lobar degeneration with TDP-43 (FTLD-TDP) type C pathology. 3 key findings →
Evidence: low
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Beyond their role in energy production, mitochondria also interact with other organelles through forming membrane contacts that serve as central hubs of cellular metabolism and signaling. 2 key findings →
Evidence: low
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This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 key findings →
Evidence: low
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Defective mitochondrial quality control is increasingly implicated in tau-mediated neurodegeneration, but how distinct tau lesions in different cell types interact with PINK1-PRKN-mediated mitophagy remains unclear. 4 key findings →
Evidence: low
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5/15 Patient:innen zeigten initial einen visuell negativen Tau-PET Scan zur Baseline, davon konvertierten vier im Follow-up zu einem Tau-positiven Befund. 5 key findings →
Participants: 15 Evidence: low
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For all 3 analytes, less than 10% difference was observed between the concentrations measured on day 0 and after 14 days of transportation and refrigeration. 3 key findings →
Evidence: low
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Tauopathies are characterized by aberrant tau structure and function, which is associated with neurodegenerative dementias, such as Alzheimer's disease, Pick's disease, and frontotemporal dementia, as well as the motor neuron disease amyotrophic lateral sclerosis. 1 key finding →
Evidence: low
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Recent evidences indicate that polymorphisms within the promoter region of the vascular endothelial growth factor (VEGF) gene may elevate the risk for Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Alzheimer disease (AD) is the leading cause of dementia globally and is defined by the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles formed by the accumulation of phosphorylated tau (p-tau). 2 key findings →
Evidence: low
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Tauopathies are a group of neurodegenerative disorders, including Alzheimer's disease, frontotemporal dementia, and progressive supranuclear palsy, characterized by the pathological accumulation of tau protein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
9 of the 733 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 →