28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
This study aims to comprehensively review the role of glial fibrillary acidic protein (GFAP) as a marker of astrocyte activation in Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The new diagnostic criteria for Alzheimer's disease (AD) include brain imaging and cerebrospinal fluid (CSF) biomarkers, with the aim of increasing the certainty of whether a patient has an ongoing AD neuropathologic process or not. 4 key findings →
Evidence: low
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Tau protein and amyloid s (Abeta), two major components of neuropathology in Alzheimer disease (AD), have been applied for establishment of more useful biomarkers and therapeutic approaches. 4 key findings →
Evidence: low
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The research focuses on the use of biomarkers to diagnose Alzheimer’s disease (AD) in living individuals. 5 key findings →
Evidence: low
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El desarrollo de biomarcadores plasmáticos ha revolucionado el diagnóstico biológico de la enfermedad de Alzheimer (EA), al permitir una detección más temprana y menos invasiva de los procesos neuropatológicos subyacentes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent progress of pharmacotherapy enabled anti-amyloid and anti-tau immunotherapy for Alzheimer disease. 5 key findings →
Evidence: low
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Objetivo: Objetivou-se sintetizar, em revisão narrativa, as evidências publicadas entre 2022–2025 sobre o potencial neuroprotetor dos análogos do GLP-1 na Doença de Alzheimer (DA). 5 key findings →
Evidence: low
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Las enfermedades neurodegenerativas representan un importante problema de salud pública debido a su creciente prevalencia y al carácter progresivo e irreversible del daño neuronal que producen. 5 key findings →
Evidence: low
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Introdução: Com o aumento da expectativa de vida e do percentual de idosos no país, também está crescendo a taxa de doenças neurodegenerativas. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ResumenLa enfermedad de Alzheimer (EA) es una enfermedad neurodegenerativa crónica que se caracteriza por la acumulación excesiva de proteína beta-amiloide y de proteína Tau fosforilada. 1 key finding →
Evidence: low
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A Doença de Alzheimer (DA) é uma enfermidade neurodegenerativa progressiva cuja detecção precoce é essencial para intervenções terapêuticas eficazes. 5 key findings →
Evidence: low
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Als blutbasierter Biomarker zur Diagnose der Alzheimer-Krankheit gilt p-Tau217. 5 key findings →
Evidence: low
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Recently-developed blood markers for Alzheimer’s (AD) detection have high accuracy but usually require ultra-sensitive analytic tools not commonly available in clinical laboratories. 4 key findings →
Participants: 136 Evidence: moderate
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By age 40 years over 90% of adults with Down syndrome (DS) have Alzheimer’s disease (AD) pathology and most progress to dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood-based biomarkers for Alzheimer’s disease (AD) have been widely studied, but direct comparisons of several biomarkers in clinical settings remain limited. 4 key findings →
Design: cross-sectional Participants: 197 Evidence: moderate
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Alzheimer disease (AD) is a heterogeneous disease with many genes are associated with AD risk. 4 key findings →
Participants: 360 Evidence: low
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There is high unmet need in dementia with Lewy bodies (DLB). 4 key findings →
Participants: 159 Evidence: high
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Blood biomarkers are increasingly used to support the diagnosis and monitoring of neurodegenerative diseases. 4 key findings →
Design: cross-sectional Participants: 5,123 Evidence: low
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These aggregated proteins contribute to the pathological and clinical heterogeneity of AD and are associated with a more rapid progression. 4 key findings →
Participants: 1,304 Evidence: low
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Increasing evidence suggests that accurate prediction of Alzheimer’s disease (AD) symptom onset requires more than amyloid- and tau-centric biomarkers such as cerebrospinal fluid (CSF) Aβ42/40, total tau and p-tau181 and plasma p-tau217. 4 key findings →
Participants: 484 Evidence: low
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In neurodegenerative diseases, the diagnostic value of α-synuclein seed amplification assay (αSAA) in routine clinical practice and its relationship with cognitive performance and fluid biomarkers remains incompletely characterized. 4 key findings →
Participants: 398 Evidence: moderate
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We investigated whether vascular and lifestyle factors are associated with AD plasma and imaging biomarkers in midlife. 4 key findings →
Participants: 1,406 Evidence: low
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Blood-based biomarkers could transform Alzheimer disease (AD) detection by enabling scalable, less invasive assessment of underlying pathology, yet their applicability across globally diverse populations remains uncertain. 4 key findings →
Design: meta-analysis Evidence: high
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Alzheimer disease (AD) pathology begins 15–20 years before clinical symptoms, necessitating non - invasive biomarkers for early diagnosis. 4 key findings →
Participants: 120 Evidence: low
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INTRODUCTIONNovel capillary-blood collection methods have not yet been evaluated for a wide range of central nervous system (CNS) and neurodegenerative disease-related proteins. 2 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 →