Acute cerebrovascular events once dominated efforts to protect the brain from cardiovascular disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Synthetic images were visually consistent, producing plausible negative and positive patterns while preserving continuity in the sagittal plane. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) destroys brain cells and the patient’s memory is lost as a result of a progressive and incurable neurodegenerative disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The pathological activation of AD microglia significantly amplifies endogenous aging characteristics. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
HIIT alone and in combination with CBD treatment significantly improved cognitive impairment induced by AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tauopathies are a group of neurodegenerative disorders, including Alzheimer's disease, frontotemporal dementia, and progressive supranuclear palsy, characterized by the pathological accumulation of tau protein. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a known risk factor for delirium. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Six key themes were identified: Inadequate preparation, guidance and access to appropriate resources; Taboo and misunderstanding: talking about death; Dementia as a terminal illness and the role of palliative care; Key time points, critical events and decisions; Planning ahead not in reality; Family issues and dynamics. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Excess salt intake is one of the relevant dietary determinants of elevated blood pressure and hypertension, with a direct impact on cardiovascular risk. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer Disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β deposition, tau pathology, synaptic dysfunction, neuronal injury and cerebral atrophy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ADAM10 plays a fundamental role in brain function, and sufficient studies support its involvement in AD pathogenesis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Introducción: La neuroinflamación ha adquirido creciente relevancia en la fisiopatología de la enfermedad de Alzheimer por su interacción con la acumulación de β-amiloide, la patología tau, la disfunción sináptica y la neurodegeneración. Microglía, astrocitos y múltiples vías de señalización inmunitaria constituyen potenciales dianas terapéuticas. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The approval of lecanemab and donanemab represents a watershed moment in Alzheimer Disease (AD) treatment, yet clinicians face a novel challenge: guiding patients through treatment selection when head-to-head comparative data are absent. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Yearly costs of evolocumab were $6,840. Donanemab was more expensive at $32,000. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is the most widespread neurodegenerative disorder and a leading cause of dementia seen in clinical practice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
controversias de los tratamientos de la enfermedad de Alzheimer» In response to 'Advances and controversies in the treatments of Alzheimer's disease' Sr. Editor, Felicitamos a la Dra.M. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is a major health issue of global concern whereby there are minimal treatment options. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The review further discusses AI-driven nanomedicine optimization and advanced human-relevant models, including brain-on-a-chip systems and three-dimensional (3D) bioprinting, as tools to improve translational prediction. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Perspectivas futuras O mesmo princípio de modulação glial pode ser aplicado em cenários de morte clínica (parada cardiorrespiratória). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This diploma thesis presents the work carried out during 6 months within the Laboratory directed by Professor Millet, written under the supervision and with the support of Dr. Benjamin Tournier and Silvia Braconi Quintaje. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
認知症を有する人のためのアドバンス・ケア・プランニング（ACP）では，意思決定能力の揺らぎを前提に，「過去」の意思と「現在」の意向を統合し，非言語的サインも含めて本人の推定意思をくみ取ることが重要である．家族を本人の想いを伝える代弁者として位置づけ，その心理的負担を医療・ケアチームが支える必要がある．また，関係依存性自律を踏まえ，多職種協働で本人中心の対話を継続することが求められる．さらに，想いのかけらを情報通信技術（ICT）等で共有し，ACPを組織的に実施する体制整備が重要である． 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our results suggest that in areas like upstate New York, where agricultural land uses are dominant, individual scale factors are the most influential. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study examines how users’ preferences for spatial elements in neighborhood parks influence satisfaction and assesses the moderating role of urban density in this relationship. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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.
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 30,580 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.
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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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