28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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Dementia, the most common subtype of which is Alzheimer’s disease, represents a significant global and social health challenge. 1 key finding →
Evidence: low
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Η νευρωνική εκφύλιση και δυσλειτουργία αποτελούν χαρακτηριστικά γνωρίσματα των νευροεκφυλιστικών ασθενειών. Σημαντική πρόκληση είναι η ανάπτυξη αξιόπιστων διαγνωστικών εργαλείων που θα επιτρέπουν την έγκαιρη διάγνωση των νόσων αυτών. Πρώτος στόχος της παρούσας διδακτορικής διατριβής είναι ο ποσοτικός προσδιορισμός επιλεγμένων πρωτεϊνικών βιοδεικτών στο εγκεφαλονωτιαίο υγρό (ΕΝΥ) και στο αίμα, με σκοπό την υποστήριξη της διαφορικής διάγνωσης διαφόρων νευροεκφυλιστικών ασθενειών. Εφαρμόστηκαν μονοπλεκτικές δοκιμασίες για τον εντοπισμό του uPAR σε ασθενείς με σποραδική νόσο Creutzfeldt-Jakob, καθώς και των TAU, α-synuclein (α-syn), YKL-40 σε ασθενείς με συνουκλεϊνοπάθειες. Η έλλειψη ευαισθησίας και ειδικότητας των μονοπλεκτικών δοκιμασιών οδήγησε στην αξιοποίηση της πολυπλεκτικής πλατφόρμας SIMOA τεσσάρων βιοδεικτών (GFAP, NfL, TAU, UCH-L1), σε δύο διαφορετικές κλινικές κοόρτες. Στους ασθενείς με νόσο Alzheimer (AD) και μετωποκροταφική άνοια (FTD), ο βιοδείκτης με την καλύτερη διαγνωστική απόδοση ήταν ο UCH-L1 στο ΕΝΥ, με τιμές διαχωρισμού στα >1260 pg/mL για AD και >1052 pg/mL για FTD. Η NfL στο ΕΝΥ έδειξε καλή διαγνωστική ακρίβεια για τη διάκριση ασθενών με AD και FTD από υγιείς μάρτυρες, με τιμή διαχωρισμού >688,8 pg/mL και >463,9 pg/mL, αντίστοιχα. Η TAU στο ΕΝΥ εμφάνισε τη δεύτερη καλύτερη απόδοση μετά το UCH-L1 για τη διάκριση των AD από μάρτυρες, με τιμή διαχωρισμού >137,0 pg/mL, ενώ έδειξε καλή ακρίβεια και στη διάκριση των AD από τους FTD. Επίσης, καλή διαγνωστική ικανότητα παρατηρήθηκε στη διάκριση FTD από μάρτυρες με τιμή διαχωρισμού >111,3 pg/mL. Τέλος, η GFAP στο ΕΝΥ παρουσίασε μετρίου βαθμού ακρίβεια στη διάκριση AD από ομάδα μαρτύρων με τιμή διαχωρισμού >5942 pg/mL. Στη Σκλήρυνση κατά πλάκας (MS) και στο Kλινικά μεμονωμένο σύνδρομο (CIS), η NfL ορού και ΕΝΥ έδειξε μέτρια διαγνωστική ακρίβεια στη διάκριση των MS από τους μάρτυρες, με τιμές διαχωρισμού >5,909 pg/mL και >453,4 pg/mL, αντίστοιχα. Η GFAP ορού παρουσίασε μέτρια διακριτική ικανότητα με τιμή διαχωρισμού >48,08 pg/mL στους MS έναντι των υγιών. Ενώ τέλος η TAU ήταν ο βιοδείκτης με την καλύτερη απόδοση στη διάκριση MS / CIS από τους μάρτυρες, με τιμή διαχωρισμού στον ορό >0,5823 / >0,5950 pg/mL, αντίστοιχα, ενώ στο ΕΝΥ <76,47 / <75,26 pg/mL, αντίστοιχα. Δεύτερος στόχος της μελέτης, είναι η διερεύνηση του ρόλου των νευρωνικών εξωσωμάτων στην παθογένεση και εξάπλωση των νευροεκφυλιστικών ασθενειών (με έμφαση στη νόσο Prion). Για τον σκοπό αυτό αξιοποιήθηκε παθολογικό μοντέλο μυός RML, το οπ 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Biomarkers in cerebrospinal fluid (CSF) are being used increasingly to diagnose early Alzheimer's disease (AD). 4 key findings →
Evidence: low
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This study aimed to assess the diagnostic contribution of Fluorodeoxyglucose Positron Emission Tomography (FDG-PET) in neurodegenerative dementias presenting with language-predominant symptoms, with or without accompanying behavioral changes, and to evaluate the correspondence between PET-derived metabolic patterns and cerebrospinal fluid (CSF) biomarkers. 4 key findings →
Evidence: low
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The dominant research paradigm for Alzheimer's disease has focused on amyloid-beta plaqueremoval for over three decades, producing no curative therapy despite billions of dollars ofinvestment. 2 key findings →
Evidence: low
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Alzheimer disease (AD) is no longer viewed only as a clinical syndrome of memory impairment but as a biological disease continuum driven by interacting amyloid-β, tau, glial, vascular, metabolic, and synaptic mechanisms. 5 key findings →
Evidence: low
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A doença de Alzheimer (DA) representa a principal causa de demência no mundo, caracterizando-se por um processo neurodegenerativo progressivo associado ao comprometimento cognitivo e funcional. 5 key findings →
Evidence: low
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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
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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
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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
Full summary, score breakdown and related studies → Original source Free full text
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
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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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10 of the 3,555 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →