27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Robust concordance between CSF biomarkers and amyloid PET visual status was observed (for Aβ42/Aβ40, AUC: 0.90; 95% CI: 0.83-0.97; p < 0.0001), confirming CSF biomarkers as a reliable alternative to amyloid PET in these studies. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma pTau217R matched CSF eMTBR-tau243 and outperformed MTBR-tau243. 5 key findings →
Participants: 242 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest that the plasma Aβ42/Aβ40 may be useful in identifying individuals with very low levels of amyloid pathology, whereas p-tau, GFAP, and NfL may be useful in staging disease progression. 3 key findings →
Design: longitudinal study Participants: 784 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An accurate blood test for Alzheimer's disease that is sensitive to preclinical proteinopathy and cognitive decline has clear implications for early detection and secondary prevention. 2 key findings →
Design: cohort study Participants: 165 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. 2 key findings →
Design: longitudinal study Participants: 1,612 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found that the cognitively unimpaired amyloid-β-negative individuals had significant longitudinal tau accumulation confined to the PET Braak-like stage I (3.9%) and II (2.8%) areas. 4 key findings →
Design: longitudinal study Participants: 125 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 showed the strongest individual association with Aβ PET status (area under the curve [AUC], 0.85). 5 key findings →
Design: cohort study Participants: 1,407 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Combining plasma p-tau with Aβ42 or the Aβ42/40 ratio reduced the intermediate zone. 5 key findings →
Design: cross-sectional Participants: 326 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The best-performing MRI-free approaches had high continuous and dichotomous agreement with MRI-dependent SUVRs for Aβ PET and temporal flortaucipir (R2 ≥0.95; ± agreement ≥92%) and for Alzheimer's disease-related effect sizes; agreement was slightly lower for entorhinal flortaucipir and longitudinal slopes. 2 key findings →
Design: longitudinal study Participants: 1,290 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There were 571 participants in the normal cognition group, 625 participants in the subjective cognitive decline group, 155 participants in the objectively defined subtle cognitive decline group, 501 participants in the mild cognitive impairment group, 471 participants in Alzheimer's disease group, and 128 participants with cognitive impairment from other known causes. 5 key findings →
Design: longitudinal study Participants: 4,386 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma amyloid-β peptide concentration has recently been shown to have high accuracy to predict amyloid-β plaque burden in the brain. 2 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Understanding the exact pathophysiological mechanisms underlying the involvement of triggering receptor expressed on myeloid cells 2 (TREM2) related microglia activation is crucial for the development of clinical trials targeting microglia activation at different stages of Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Participants: 1,001 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Participants with CIND displayed lower perfusion in the PCC+PCu relative to participants who were CN, but there was no statistically significant difference between the groups in amyloid burden in this region. 5 key findings →
Design: case-control study Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CL was associated with syndromic (F = 4.42, p = 0.014) and etiological diagnosis (F = -12.66, p < 0.001), with Alzheimer's disease (AD) patients showing the highest amyloid burden (62.9 ± 27.5), followed by dementia with Lewy bodies (DLB) (25.3 ± 35.5) and cardiovascular disease (CVD) (16.7 ± 24.5), and finally frontotemporal lobe degeneration (FTLD) (5.0 ± 17.22, t = -12.66, p < 0.001). 4 key findings →
Design: longitudinal study Participants: 157 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Aβ-PET was abnormal in 81 participants from J-TRC and 71 participants from BioFINDER. 2 key findings →
Design: cross-sectional Participants: 474 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid chronicity provides unique information about cognitive decline and neurofibrillary tangle development and may be useful to investigate preclinical Alzheimer's disease. 2 key findings →
Design: longitudinal study Participants: 257 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Subtraction MRI has potential as a visual aid increasing the sensitivity of ARIA-E assessment. 3 key findings →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results encourage an independent validation cohort study to confirm the indication that the plasma Aβ 1-40 /Aβ 1-42 ratio, assessed via Simoa, may improve future standard of care and clinical trial design. 2 key findings →
Design: cohort study Participants: 276 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Primary include several amyloid PET measurements (Centiloid, SUVr, BPND , R1 ), and secondary are their changes from baseline, relationship to other amyloid markers (cerebrospinal fluid and visual assessment), and predictive value of AD-related decline. 2 key findings →
Design: cohort study Participants: 2,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found that a higher PGS was associated with higher rates of tau-PET accumulation, in particular at elevated amyloid-PET levels. 4 key findings →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source
53/310 (17.1%) subjects were classified as Focal-FMM. 5 key findings →
Design: longitudinal study Participants: 310 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Principal component analysis identified patterns of variation in baseline and longitudinal measures of tau uptake and volume that were significantly different across phenotypes. 2 key findings →
Design: longitudinal study Participants: 57 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Progressive tau accumulation may be more prominent in ε4 carriers, particularly in the medial and lateral temporal cortices. 1 key finding →
Design: longitudinal study Participants: 272 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Florbetaben scans were assessed visually and quantitatively, and results were compared with amyloid plaque scores. 3 key findings →
Design: open-label trial Participants: 82 Evidence: low
Full summary, score breakdown and related studies → Original source
At baseline, 283 were Plasma-/PET-, 97 Plasma+/PET-, 76 Plasma-/PETLow, and 51 Plasma+/PETLow. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 27,380 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.
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 →