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
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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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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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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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A Doença de Alzheimer (DA) é a principal causa de demência em idosos, causada pelo acúmulo de β-amiloide e emaranhados neurofibrilares no cérebro. 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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Các bệnh lý như lao và Alzheimer đòi hỏi phát hiện sớm với độ nhạy cao để can thiệp kịp thời, tuy nhiên các kỹ thuật hiện nay như ELISA, PCR còn hạn chế về chi phí và độ nhạy. Những tiến bộ gần đây trong công nghệ nano cho thấy hạt nano vàng vỏ đồng kết hợp sinh phẩm tái tổ hợp (protein hoặc aptamer) có thể khuếch đại tín hiệu màu, mở ra triển vọng cho chẩn đoán sớm siêu nhạy. Bài tổng quan này phân tích cơ chế kỹ thuật xét nghiệm kháng nguyên bằng sự hình thành vỏ nano đồng trên hạt vàng, trong đó ion Cu²⁺ được khử bởi natri ascorbate trên bề mặt AuNPs với vai trò ổn định của polyethylenimine, tạo cấu trúc Au-Cu đa giác giúp tăng cường tín hiệu plasmon. 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
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The diagnostic significance of tau proteins in cerebrospinal fluids (CSF) has been described in many cases of dementia of Alzheimer type (AD). 4 key findings →
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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A doença de Alzheimer (DA) configura-se como a principal causa de demência em idosos, se tornando um dos maiores desafios da medicina moderna devido à sua alta prevalência e o impacto social associado. 5 key findings →
Evidence: low
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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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medRxiv
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2024-10-27
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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Research Square
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2021-10-21
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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Research Square
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2026-08-14
There is high unmet need in dementia with Lewy bodies (DLB). 4 key findings →
Participants: 159
Evidence: high
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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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medRxiv
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2026-08-11
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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medRxiv
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2026-08-05
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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medRxiv
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2026-04-01
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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medRxiv
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2026-04-23
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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medRxiv
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2026-04-17
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
medRxiv
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2026-05-18
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
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Research Square
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2026-04-09
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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16/100
⚠ Preprint — not yet peer-reviewed
alzhub usefulness score 16 out of 100.
·
medRxiv
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2026-09-29
Symptomatic DIAD participants who had been treated for ∼ 4 years with anti-Aβ monoclonal antibodies (gantenerumab, n=4 or solanezumab, n=4) were compared with untreated, symptomatic DIAD mutation carriers (n=40) and with age-relevant non-DIAD controls with modest or no plaque pathology (n=18). 5 key findings →
Evidence: low
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How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 30,180 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.