Higher CSF NfL was associated with decreasing microstructural integrity and WMH. 5 key findings →
Design: longitudinal study Participants: 536 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We found eight flortaucipir covariance patterns which were reproducible and overlapped with relevant gene expression maps. 5 key findings →
Participants: 418 Evidence: low
Full summary, score breakdown and related studies → Original source
GMM-based cutoffs classified less subjects as T+, mainly in the A- CN (<3.4% vs >28.5%) and A+ CN (<14.5% vs >42.9%) groups and showed higher agreement with visual rating (ICC=0.91 vs ICC<0.62) than published cutoffs. 3 key findings →
Participants: 269 Evidence: low
Full summary, score breakdown and related studies → Original source
Elevated CSF p-tau181 and cortical 18F-PI-2620 binding was characteristic for AD while normal CSF p-tau181 with elevated subcortical 18F-PI-2620 binding was characteristic for 4RTs. 18F-PI-2620-assessed posterior cortical hypoperfusion could be used as an additional neuronal injury biomarker in AD. 5 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Accurate staging of Alzheimer's disease (AD) pathology is crucial for therapeutic trials and prognosis, but existing fluid biomarkers lack specificity, especially for assessing tau deposition severity, in amyloid-beta (Aβ)-positive patients. 2 key findings →
Participants: 136 Evidence: low
Full summary, score breakdown and related studies → Original source
Based on retrospective data, we develop personalized risk estimates for MCI patients. 4 key findings →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
There were significant associations (p < 0.05) between the NPI variables (total score, Affective factor) and entorhinal and precuneus tau across all participants. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
48/100
Our cohort was composed of 59 cognitively normal participants and 10 cognitively impaired individuals. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that primarily affects the elderly population. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To elucidate the relationship between cerebrospinal fluid (CSF) total-tau (T-tau) and phosphorylated tau (P-tau) with the tau PET ligand 18 F-AV-1451 in Alzheimer's disease (AD), we examined 30 cognitively healthy elderly (15 with preclinical AD), 14 prodromal AD, and 39 AD dementia patients. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current technological advancements in clinical and research settings have permitted a more intensive and comprehensive understanding of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) pathology is estimated to develop many years before detectable cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recent failures of potential disease-modifying drugs for Alzheimer's disease (AD) may reflect the fact that the enrolled participants in clinical trials are already too advanced to derive a clinical benefit. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A prespecified structure–reserve–glial profile captured reproducible cognitive variation beyond measured Alzheimer disease molecular pathology across two cohorts. 1 key finding →
Design: longitudinal study Participants: 436 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Complement-mediated neuroinflammation has been implicated in Alzheimer’s disease (AD), but its role during the pre-symptomatic phase of the disease remains unclear. 4 key findings →
Participants: 708 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid regional extent and tau PET were associated with different features of dyadic CFI data: reporter balance and CFI burden across reporters, respectively. 4 key findings →
Design: cross-sectional Participants: 1,686 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease pathology and cognitive outcomes frequently diverge, yet current single-axis definitions cannot identify resilient (high pathology, preserved cognition) and resistant (high risk, low pathology) subgroups reliably at scale, obscuring the mechanisms that uncouple pathological burden from cognitive decline. 2 key findings →
Participants: 1,009 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →