The antemortem diagnosis of Alzheimer disease (AD) requires time-consuming and costly procedures. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The antemortem diagnosis of Alzheimer disease (AD) requires time-consuming and costly procedures. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Cerebrospinal fluid values of total tau (T-tau) and β-amyloid 1-42 (Aβ 1-42) obtained using the Innotest enzyme-linked immunosorbent assay were transformed using a linear regression model to equivalent values obtained using the INNO-BIA AlzBio3 (xMAP; Luminex) assay. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Physical exercise may have some effect on cognition in patients with Alzheimer disease (AD). 4 key findings →
Participants: 53 Evidence: low
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Biomarker validation in a clinical cohort. 4 key findings →
Evidence: moderate
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The National Institute on Aging and Alzheimer's Association (NIA-AA) have proposed a new Research Framework: Towards a biological definition of Alzheimer's disease, which uses a three-biomarker construct: Aß-amyloid, tau and neurodegeneration AT(N), to generate a biomarker based definition of Alzheimer's disease. 4 key findings →
Participants: 27 Evidence: low
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Alzheimer disease (AD) and frontotemporal lobar degeneration (FTLD) may have overlapping clinical presentations despite distinct underlying neuropathologies, thus making in vivo diagnosis challenging. 4 key findings →
Participants: 185 Evidence: low
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Recent technical advances in peripheral blood analysis have enabled precise quantification of Alzheimer´s Disease (AD) biomarkers in the early stages of the AD continuum, in an economical, non-invasive and safe manner. 4 key findings →
Participants: 329 Evidence: moderate
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BackgroundC1q is a promoter of the classical pathway of complement and its massive expression may be associated with the development of Alzheimer's disease (AD). 2 key findings →
Participants: 1,264 Evidence: low
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Alzheimer disease (AD) is characterized by amyloid-β plaques (A), tau tangles (T), and neurodegeneration (N), collectively defining the ATN framework. 4 key findings →
Design: longitudinal study Evidence: moderate
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Postmortem demonstration of increased expression of biologically active S100B in Alzheimer's disease (AD) and its relation to progression of neuropathological changes across the cortical regions suggests involvement of this astrocytic cytokine in the pathophysiology of AD. 4 key findings →
Evidence: low
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Showa University Karasuyama Hospital, Tokyo, Japan. 4 key findings →
Participants: 106 Evidence: low
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Clinical trials of disease modifying drugs for Alzheimer's disease (AD) in patients with mild cognitive impairment (MCI) might benefit from enrichment with true AD cases. 4 key findings →
Evidence: low
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The trajectories of depression and apathy (measured with the Neuropsychiatric Inventory or its questionnaire) were separately modeled using growth mixture models for two cohorts (National Alzheimer's Coordinating Center, NACC, n = 22 760 and Alzheimer's Disease Neuroimaging Initiative, ADNI, n = 1 733). 4 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common cause of dementia in the elderly, and the fourth leading cause of death in the United States. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among 5712 adults (mean [SD] age, 63.47 (8.15) years; unweighted 3663 [53.92%] female), higher ln(ptau-181) was associated with ECog-12 memory (unstandardized β = 0.088; 95% CI, 0.005-0.170). 5 key findings →
Design: cross-sectional Participants: 5,712 Evidence: moderate
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Alzheimer's disease (AD) and frontotemporal dementia (FTD) are the most common forms of dementia globally. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is characterized by the pathological accumulation of amyloid plaques and hyperphosphorylated tau proteins, leading to disruptions in synaptic transmission and neural circuit alterations. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The SorLA protein, encoded by the Sortilin-related receptor 1 ( SORL1 ) gene, is a major player in Alzheimer’s disease (AD) pathophysiology. 4 key findings →
Participants: 30 Evidence: low
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Inflammatory responses are characterized by the activation of immune cells, while inflammatory biomarkers intricately interact with the immune system. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma Aβ 42/40 , p‐tau‐181, and NfL differ in those with CAA and together can discriminate CAA from healthy controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroaxonal damage underlies permanent disability in various neurological conditions, both neuroautoimmune and neurodegenerative. 5 key findings →
Design: narrative review Evidence: low
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CSF and plasma SNAP25 were positively correlated, but no correlation was observed for VAMP2 in these matrices. 5 key findings →
Participants: 80 Evidence: low
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Alzheimer's disease (AD) is characterized by progressive memory loss and cognitive decline, significantly impairing the daily life of elderly individuals. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early-stage Alzheimer's disease (AD) remains difficult to assess using conventional linguistic or cognitive assessments, which often overlook subtle and individualized disruptions in speech. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Revealing the relationship between dysfunctional genes in blood and brain tissues from patients with Alzheimer's Disease (AD) will help us to understand the pathology of this disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 939 studies in this tag that have a study page, 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events