27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
With the emergence of Alzheimer's disease (AD) disease-modifying therapies, identifying patients who could benefit from these treatments becomes critical. 1 key finding →
Participants: 1,422 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Despite significant progress, applications of astrocyte biomarkers in AD remain in their early days. 4 key findings →
Design: systematic review Participants: 3,204 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In a large cohort of cognitively unimpaired individuals enrolled in a Phase 3 clinical trial and companion observational study, these findings confirm that higher baseline levels of amyloid and tau markers are associated with increased rates of cognitive decline and progression to functional impairment. 5 key findings →
Design: longitudinal study Participants: 583 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Of 236 eligible participants screened, 43 were excluded. 2 key findings →
Design: longitudinal study Participants: 142 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
APOE4 confers greater AD risk in women. 5 key findings →
Design: case-control study Participants: 5,496 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Furthermore, plasma p-tau231 was significantly increased in amyloid-β PET quartiles 2-4, whereas CSF p-tau217 and plasma p-tau181 increased only at quartiles 3-4 and 4, respectively. 2 key findings →
Participants: 588 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma tau partly reflects AD pathology, but the overlap between normal aging and AD is large, especially in patients without dementia. 3 key findings →
Design: longitudinal study Participants: 179 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Smoothing splines demonstrated that earliest plasma p-tau181 changes occurred even before amyloid-β markers reached abnormal levels, with greater rates of change correlating with increased amyloid-β pathology. 4 key findings →
Design: prospective cohort Participants: 1,067 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We tested the hypothesis that plasma neurofilament light chain (NfL) identifies asymptomatic carriers of familial frontotemporal lobar degeneration (FTLD)-causing mutations at risk of disease progression. 4 key findings →
Design: longitudinal study Participants: 277 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Midlife p-tau181 was associated with faster 11-year memory decline beginning 20 years later in the ARIC cohort, which underscores a potentially long prodromal phase of cognitive decline that could precede dementia onset. 5 key findings →
Design: prospective cohort Participants: 920 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recently approved anti-amyloid immunotherapies for Alzheimer's disease (AD) require evidence of amyloid-β pathology from positron emission tomography (PET) or cerebrospinal fluid (CSF) before initiating treatment. 4 key findings →
Design: cohort study Participants: 6,896 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cognitive-motor dual-task training was more beneficial than single-task training alone in improving broader domains of cognitive functions of elderly persons, and the improvement was not directly due to modulating Aβ metabolism. 4 key findings →
Participants: 27 Evidence: high
Full summary, score breakdown and related studies → Original source
Based on integrated review of laboratory, electrocardiogram, adverse events, and MRI, AAB-003 was safe and well tolerated up to 8 mg/kg for up to 91 weeks (FIH and extension trials) in patients with mild to moderate AD. 4 key findings →
Design: open-label trial Participants: 52 Evidence: high
Full summary, score breakdown and related studies → Original source
These findings support the short-term efficacy and safety of Lecanemab in early AD and highlight plasma biomarkers as a treatment-responsive biomarker. 3 key findings →
Design: cohort study Participants: 68 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mixed-effect models assessed rates of memory decline in relation to baseline plasma p-tau181, and whether plasma p-tau181 significantly predicted memory decline beyond widely available clinical and genetic data (age, sex, years of education, cardiovascular and metabolic conditions, and APOE ε 4 status). 5 key findings →
Design: longitudinal study Participants: 604 Evidence: moderate
Full summary, score breakdown and related studies → Original source
However, because these biomarkers are strongly associated with the emergence of Aβ pathology, it is difficult to determine the contribution of insoluble tau aggregates to the plasma p-tau signal in blood. 5 key findings →
Design: longitudinal study Participants: 1,294 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Potential DMT candidates at Butler MAP (n = 50), primarily diagnosed with mild cognitive impairment (n = 29 [58%]) or mild dementia (21 [42%]), were predominantly Aβ-positive (38 [76%]), and half (25 [50%]) were subsequently treated with aducanumab. 1 key finding →
Design: cohort study Participants: 150 Evidence: moderate
Full summary, score breakdown and related studies → Original source
PTau217R reliably predicts regional tau accumulation in early AD, reducing reliance on tau PET scans and broadening its clinical application. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau181/NfL can potentially be used to monitor large-scale population interventions in CU individuals. 2 key findings →
Design: longitudinal study Participants: 257 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The panel cautions users of this guideline that there is significant variability in diagnostic test accuracy and many commercially available BBM tests do not meet these thresholds, especially using a single cutoff. 1 key finding →
Design: systematic-review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The mean (SD) baseline age of 758 participants was 61.5 (6.1) years, and 424 participants [55.9%] were female. 4 key findings →
Design: cohort study Participants: 758 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neuroinflammation and cerebrovascular dysfunction are early events occurring already at presymptomatic stages of AD and contribute to disease progression. 5 key findings →
Design: longitudinal study Participants: 508 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Changes in β-amyloid (Aβ) and hyperphosphorylated tau (T) in brain and cerebrospinal fluid (CSF) precede Alzheimer's disease (AD) symptoms, making the CSF proteome a potential avenue to understand disease pathophysiology and facilitate reliable diagnostics and therapies. 5 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
In TRIAD, ALZpath p-tau217 (β = 0.45, p = 0.02) and p-tau217+Janssen (β = 0.67, p = 0.002), and in ADNI p-tau217 (β = 0.90, p = 0.002) increased faster in A+E4+. 5 key findings →
Design: longitudinal study Participants: 2,039 Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 3,069 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.
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
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.
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.
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 →