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Research

27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 876–900 of 900 studies (page 36 of 36) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 900 studies tagged csf — clear

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Each number is how many studies that link shows, with your other filters kept.

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 13,259 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Identification and functional verification of new molecular targets of blood – cerebrospinal fluid and exosomes from patients with neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 29 out of 100. Aristotle University of Thessaloniki 2026-01-01

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

Neurobiological studies of dementia--biological markers and neuroprotective strategies for Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Acta neurologica Taiwanica 2006-03-01

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

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Avanços em biomarcadores plasmáticos e do líquido cefalorraquidiano para a detecção precoce da doença de Alzheimer

✓ Peer-reviewed alzhub usefulness score 27 out of 100. Brazilian Journal of Health Review 2025-01-14

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

Full summary, score breakdown and related studies → Original source Free full text

Diagnostic performance of plasma Aβ 1-42 , Aβ 1-40 and pTau 181 in the LUMIPULSE automated platform for the detection of Alzheimer disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2023-04-26

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

Full summary, score breakdown and related studies → Original source Free full text

A head-to-head comparison of plasma biomarkers to detect biologically defined Alzheimer in a memory clinic

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 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

Full summary, score breakdown and related studies → Original source Free full text

Abnormalities in core AD biomarkers precede inflammatory and glial markers in CSF in Autosomal Dominant Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 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

Full summary, score breakdown and related studies → Original source Free full text

Routine implementation of α-synuclein Seed Amplification Assays reveals high diagnostic performance and the limited value of Alzheimer disease fluid biomarkers for detecting α-synuclein co-pathology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 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

Full summary, score breakdown and related studies → Original source Free full text

Blood biomarkers for Alzheimer disease across ethnoracial groups and healthcare settings: a systematic review and meta-analysis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 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

Full summary, score breakdown and related studies → Original source Free full text

Application of Plasma Neuron-Derived Exosome-Based Multimodal Biomarkers in the Early Diagnosis of Alzheimer's Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 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

Full summary, score breakdown and related studies → Original source Free full text

Performance of upper-arm capillary blood collection for Alzheimers disease and central nervous system biomarkers: comparison of Tasso+ and venous plasma

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-20

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

Alzheimers disease blood biomarkers reveal proteomic modules of disease progression

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-19

Alzheimers disease (AD) unfolds over decades preceding cognitive symptoms, and measuring the full scope of its molecular complexity remains difficult. 1 key finding →

Participants: 11,042 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Plasma inflammatory biomarker associations with Alzheimers disease clinical stage and CSF biomarkers: evaluation of sex effects

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-17

BackgroundAlzheimers disease (AD) is characterized by amyloid beta and tau accumulation accompanied by altered inflammatory responses. 4 key findings →

Design: cross-sectional Participants: 261 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Exploring Machine Learning Models to Uncover Pathways in ALS Pathogenesis Using Immunohistochemical Features

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-20

Hexanucleotide repeat expansions in C9orf72 are the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia, yet the predictive information contained within associated inflammatory and proteinopathy markers remains incompletely characterised. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Adult Vaccination History and Plasma Biomarker Signatures in the Asymptomatic PREVENT-AD Cohort

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-27

BackgroundEpidemiological studies increasingly associate several adult vaccinations with lower risk of Alzheimers disease (AD) and dementia, but the biological mechanisms underlying these observations remain unclear. 5 key findings →

Design: longitudinal study Participants: 192 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Genetic associations with EEG signatures in mild cognitive impairment: insights into Alzheimer's disease pathophysiology

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-28

Genome-wide genotypes were quality-controlled, imputed, functionally annotated (yielding 16,935 gene regions comprising 90,607 functional variants), and associated with latent EEG features using Bayesian reduced rank regression. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Treatment response biomarkers in early Alzheimers disease: longitudinal trajectories, sample size estimates, and the impact of progression variability

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-31

BackgroundFluid biomarkers enable the demonstration of the biological effects of novel therapies in Alzheimers disease (AD). 1 key finding →

Design: longitudinal study Participants: 65 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Proteoform-resolved neoGFAP as a diagnostic and prognostic biomarker across the TBI--MCI--AD continuum in Veterans

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-03

Service members with traumatic brain injury are at approximately two- to four-fold higher risk of Alzheimers disease or related dementias than those without such an injury, with risk increasing with injury severity. 5 key findings →

Participants: 57 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Plasma proteomics reveals stage-dependent biological remodelling in Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-14

Plasma biomarkers of amyloid-associated tau phosphorylation (T1) and established tau proteinopathy (T2) can approximate Alzheimers disease stage, but whether plasma-defined stages correspond to broader biological states is unknown. 1 key finding →

Design: cross-sectional Participants: 1,035 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Serum Brain-Derived Neurotrophic Factor Across the Human Lifespan: A Systematic Review and Meta-Analysis

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-14

BackgroundBone marrow megakaryocytes, the primary source of brain-derived neurotrophic factor (BDNF) in the blood, secrete BDNF-packed platelets into the bloodstream. 3 key findings →

Design: meta-analysis Evidence: high

Full summary, score breakdown and related studies → Original source

Association of plasma biomarkers with longitudinal change in age- and Alzheimer's disease-related brain atrophy patterns

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-17

INTRODUCTIONDetermining whether plasma biomarkers are preferentially associated with Alzheimers disease (AD)-related rather than age-related brain atrophy patterns may clarify their prognostic and diagnostic clinical use. 5 key findings →

Design: cross-sectional Participants: 818 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Physiological variability in key Alzheimer's biomarkers in amyloid-positive clinical trial cohorts and the mechanistic basis of biomarker ratios

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-21

While normalizing biomarker values by A{beta}40 or A{beta}42 reduced physiological variability for some biomarkers, the effects of the normalization were compartment-, and cohort-dependent. 5 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

A neurocognitive speech taxonomy for voice biomarkers of Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-09-25

NST showed stable cross-cohort structure (Mantel r = 0.71-0.77) and differentiated MCI (d = -0.39) and AD biomarker status (d = -0.23). 4 key findings →

Design: longitudinal study Participants: 1,479 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

From across this tag

10 of the 895 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.

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Where “Free full text” comes from

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

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 27,780 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.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →

Newest studies, as a dated timeline →    Atom feed