28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the 2-month-old mice, sonobiopsy significantly increased the normalized levels of plasma p-tau species compared with the conventional blood-based liquid biopsy (p-tau-181-to-mouse tau [m-tau] ratio: 1.7-fold increase, P = .006; p-tau-231-to-m-tau ratio: 1.4-fold increase, P = .048). 1 key finding →
Evidence: low
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There is an urgent need for objective markers of Alzheimer’s disease (AD)-related cognitive impairment in people with Down syndrome (DS) to improve diagnosis, monitor disease progression and assess response to disease-modifying therapies. 4 key findings →
Participants: 80 Evidence: moderate
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Cerebrospinal fluid (CSF) biomarkers have been increasingly studied in dementia clinical and differential diagnosis. 4 key findings →
Participants: 34 Evidence: low
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Hypercortisolemia and increased levels of hyperphosphorylated tau proteins in cerebrospinal fluid (CSF) are common features with pathogenic relevance in Alzheimer;s disease (AD). 4 key findings →
Participants: 26 Evidence: low
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Alzheimer disease (AD) is a complex neurodegenerative disorder, whose prevalence will dramatically rise by 2050. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Total tau (T-tau), tau phosphorylated at threonine 181, and β-amyloid 1-42 peptide (Aβ42) were immunoassayed in CSF samples obtained from patients with MCI enrolled in the Alzheimer's Disease Neuroimaging Initiative. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Early diagnosis of Alzheimer s disease (AD) is relevant in order to initiate symptomatic treatment with antidementia drugs. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia. 4 key findings →
Participants: 73 Evidence: low
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Cerebrospinal fluid (CSF) samples from 33 patients with Alzheimer dementia (AD), 21 patients with mild cognitive impairment who converted to AD during followup (MCI-AD), 25 patients with stable mild cognitive impairment (MCI-stable), and 16 nondemented subjects (ND) were analyzed with a chemiluminescence immunoassay to assess the levels of the mitogen-activated protein kinase ERK1/2 (extracellular signal-regulated kinase 1/2). 4 key findings →
Participants: 33 Evidence: low
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According to the amyloid, tau, neurodegeneration research framework classification, amyloid and tau positive (A+T+) mild cognitive impairment (MCI) individuals are defined as prodromal Alzheimer disease. 4 key findings →
Participants: 64 Evidence: low
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BackgroundAir pollution has been almost exclusively measured by region-level ambient exposure of particulate matter (PM) from government agencies (e.g., EPA), which does not capture the potentially large within-region variation and takes no consideration of human mobility in daily life. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is one of the pathologies that the scientific world is still desperate for. 4 key findings →
Participants: 120 Evidence: low
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The purpose of this study was to investigate whether plasma biomarkers can help to diagnose, differentiate from Alzheimer disease (AD), and stage cognitive performance in patients with positron emission tomography (PET)-confirmed primary age-related tauopathy, termed tau-first cognitive proteinopathy (TCP) in this study. 4 key findings →
Participants: 55 Evidence: low
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As disease-modifying therapies become available for Alzheimer's disease (AD), detection of AD in early stages of illness (mild cognitive impairment [MCI], early dementia) becomes increasingly important. 4 key findings →
Participants: 185 Evidence: moderate
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The lack of significant results for moderation effects of the targeted epigenetic markers in our pilot study were likely due to the small sample size. 5 key findings →
Participants: 812 Evidence: moderate
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Alzheimer disease (AD) diagnosis is confirmed using a medley of modalities, such as the detection of amyloid-β (Aβ) neuritic plaques and neurofibrillary tangles with positron electron tomography (PET) or the appraisal of irregularities in cognitive function with examinations. 3 key findings →
Participants: 53 Evidence: low
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Alzheimer disease plasma biomarkers have emerged as minimally invasive, cost-effective tools for early diagnosis and disease monitoring yet their stability under common "real world" pre-analytical conditions remains incompletely characterized. 3 key findings →
Participants: 12 Evidence: low
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Vascular burden influences NfL levels, particularly in amyloid‐negative individuals. 5 key findings →
Participants: 371 Evidence: moderate
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We have successfully generated specific high affinity monoclonal antibodies against p -Tau217, p -Tau205, and N-terminus GFAP and have confirmed that these antibodies have the necessary specificity and sensitivity for the Simoa platform. 2 key findings →
Evidence: moderate
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A total of 143 patients with cognitive concerns were included who underwent a PrecivityAD2 test as part of their clinical evaluation. 5 key findings →
Participants: 4,000 Evidence: moderate
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Early and accurate prognosis of Alzheimer’s disease (AD) remains limited by current biomarkers, which are often invasive, require expensive equipment, or fail to predict individual trajectories of cognitive decline. 2 key findings →
Participants: 459 Evidence: moderate
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Fourteen studies met eligibility criteria, covering populations from healthy controls to individuals with subjective cognitive decline, MCI, AD, and other dementias. 5 key findings →
Evidence: low
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Utilizing machine learning, we identify a 12-protein panel from cerebrospinal fluid proteomic datasets. 5 key findings →
Evidence: low
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While the β-secretase BACE1 is responsible for the rate-limiting initial step to generate amyloid-β (Aβ) peptides, BACE1 inhibitor clinical trials have been halted due to a lack of efficacy and/or safety concerns at symptomatic/prodromal stages of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 3,322 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 10. The same 10 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 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 →