LIUS was safe and demonstrated both cognitive improvement and reduced amyloid deposition in early‐stage AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurodegeneration status was correctly identified in 78.8% (119/151) of amyloid-negative patients through visual rating, compared to 67.5% (102/151) using logistic regression. 5 key findings →
Participants: 379 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In older adults, temporal [18F]PI-2620 binding was higher in women (β = 0.543, P < 0.001) and APOE4 carriers (β = 0.395, P = 0.030) and was positively associated with plasma p-tau217 (β = 0.22, P = 0.008). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PRS correlated positively with log-NFL (r = 0.31, p = 0.004) and inversely with N3 duration (r = −0.26, p = 0.017). 5 key findings →
Design: cross-sectional Participants: 84 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
38/100
Participants’ motivations for testing and long-term adaptation to the results were strongly shaped by cognitive concerns and personal experiences of dementia in relatives. 5 key findings →
Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Lecanemab is a humanized IgG1 monoclonal antibody binding with high affinity to protofibrils of amyloid-beta (Aβ) protein. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Here the current and emerging roles of brain positron emission tomography (PET) in Alzheimer's disease (AD) in the era of anti-amyloid-β antibody therapy, with a focus on clinical applications, methodological considerations, and future perspectives were reviewed. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent advances in Blood-Based Biomarkers (BBMs) are transforming the diagnostic landscape of Alzheimer Disease (AD), with plasma p-tau217 emerging as a highly accurate and scalable diagnostic marker of AD pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
P. gingivalis-induced periodontitis dampened hippocampal Bmal1 rhythms, lowered p-AKT, activated glia, and elevated Aβ and interleukin 1β (IL-1β). 4 key findings →
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 fisiopatologia envolve, entre outros mecanismos, o acúmulo cerebral de β-amiloide, associado a alterações da proteína tau, sua hiperfosforilação e formação de emaranhados neurofibrilares, contribuindo para a disfunção sináptica e a perda neuronal. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The NfL assay met analytical criteria, with precision demonstrating coefficients of variation <3% across runs, a lower limit of quantification of 3.10 pg/mL, linearity with <12% deviation, and <10% interference. 5 key findings →
Participants: 20 Evidence: low
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Agreement between Syngo.via and MIMneuro varied by region. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
To evaluate plasma p-tau217 ability to detect pre-symptomatic Alzheimer disease (AD) in ethnoracially diverse cognitively normal individuals. 1 key finding →
Evidence: low
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To determine the relationship between regional brain edema caused by anti-amyloid monoclonal antibody therapy (ARIA-E) and the degree of regional β-amyloid (Aβ) positron emission tomography (PET) signal reduction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
A Doença de Alzheimer (DA) é a principal causa de demência no mundo, caracterizada por processos neurodegenerativos progressivos que comprometem cognição, comportamento e funcionalidade. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Women have twice the dementia risk compared with men. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Theranostics—the use of diagnostic and therapeutic drugs that target the same molecular marker of disease—extends beyond the paradigm of radiopharmaceutical drug pairs used in oncologic settings (e.g., somatostatin receptor subtype 2 and prostate-specific membrane antigen theranostics) to other 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Anemia and iron deficiency are common in older adults, yet their relevance to blood biomarkers for Alzheimer disease (AD) remains underappreciated. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
12.05.2026: Debatt - En enkel blodprøve kan nå påvise fosforylert tau-protein 217 (p-tau217) – et biologisk tegn på Alzheimers sykdom, som kan være til stede mange år før de første symptomene viser seg. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A 77-year-old woman with mild cognitive impairment was referred to 18F-florbetapir positron emission tomography (PET) to assess the indication of a disease-modifying drug against Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
The most successful amyloid-targeting treatments achieve modest plaque reduction with marginal clinical benefit and significant adverse effects. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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 (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
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
- Randomized / 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
- Multicenter 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 32,180 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.
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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.
1,045 records (3.2% of the library) are not peer-reviewed — 966 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
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