30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Second, we examined volumetric associations with amyloid (amyloid positive, tau negative versus control) and tau in the presence of amyloid (amyloid positive, tau positive versus amyloid positive, tau negative) across 52 brain areas. 5 key findings →
Design: meta-analysis Participants: 306 Evidence: high
Full summary, score breakdown and related studies → Original source
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
Increasing evidence suggests an important role of liver function in the pathophysiology of Alzheimer disease (AD). 4 key findings →
Design: cohort study Participants: 1,581 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
An increased tau positron emission tomography (PET) signal in the medial temporal lobe (MTL) has been observed in older individuals in the absence of amyloid-β (Aβ) pathology. 4 key findings →
Design: cohort study Participants: 1,093 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Data from deformation-based magnetic resonance imaging morphometry demonstrated a Parkinson's disease-specific brain network had more atrophy in the diffuse malignant subtype, with the mild motor-predominant subtype having the least atrophy. 4 key findings →
Design: longitudinal study Participants: 223 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →
Design: longitudinal study Participants: 2,609 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The amyloid/tau/neurodegeneration (A/T/N) framework uses cerebrospinal fluid (CSF) levels of total tau (tTau) as a marker of neurodegeneration and CSF levels of phosphorylated tau 181 (pTau181) as a marker of tau tangles. 4 key findings →
Design: cohort study Participants: 465 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Biomarkers were extracted from a total of 42 participants with longitudinal time points representing 164 imaging volumes. 5 key findings →
Design: longitudinal study Participants: 24 Evidence: moderate
Full summary, score breakdown and related studies → Original source
It remains unclear which risk factors accelerate brain atrophy along with a progression from normal cognition to mild cognitive impairment (MCI). 4 key findings →
Design: cohort study Participants: 185 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) is primarily associated with accumulations of amyloid plaques and tau tangles in gray matter, however, it is now acknowledged that neuroinflammation, particularly in white matter (WM), significantly contributes to the development and progression of AD. 4 key findings →
Design: cross-sectional Participants: 310 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Virtually identical t-tau/Aβ42 cut-points (∼0.54) performed best in both test cohorts and with similar accuracy (areas under ROC curve [AUCs] [A/B: 0.95; C: 0.94]). 3 key findings →
Participants: 138 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Normal E4 carriers with SMC show altered AD-related CSF and FDG-PET measures. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Positive cerebrospinal fluid (CSF) biomarkers of tau and amyloid beta42 suggest possible active underlying Alzheimer's disease (AD) including neurometabolic dysfunction and neurodegeneration leading to eventual cognitive decline. 4 key findings →
Design: cohort study Participants: 82 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Concentration of CSF pT217/T217 had low predictive error (average error: 13%), but also a low predictive range (ceiling 63 Centiloids). 5 key findings →
Participants: 346 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma pTau181 may have utility as a biomarker of AD pathophysiology and as a noninvasive screener for elevated brain Aβ.
Full summary, score breakdown and related studies → Original source Free full text
Voxel-based analyses demonstrated significant negative correlations between CSF tau and ptau(181) levels and CMRglu in the posterior cingulate, precuneus, and parahippocampal regions. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Comparing the discordant CSF results of each patient with the cerebral amyloid-PET results, we found that in the group with Aβ1 - 42+ and p-tau-CSF values, the amyloid-PET was positive in 51.2% and negative in 48.8% of patients, while in the group with Aβ1 - 42-and p-Tau+ CSF values, the amyloid-PET was positive in 52.6% of patients and negative in 47.4% of them. 4 key findings →
Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source
The two primary molecular pathologies in Alzheimer's disease are amyloid-β plaques and tau-immunoreactive neurofibrillary tangles. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cross-sectional data, including CSF analytes, molecular imaging of cerebral fibrillar β-amyloid (Aβ) with PET using the [ 11 C] benzothiazole tracer Pittsburgh compound B (PiB), MRI-based brain structures, and clinical/cognitive outcomes harmonized from 8 studies, collectively involving 3,284 cognitively normal individuals 18 to 101 years of age, were analyzed. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This prospective, observational study enrolled patients with early AD undergoing Alzheimer's biomarker analysis and matched controls. 4 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
White matter hyperintensities (WMH) correlate with Alzheimer disease (AD) biomarkers cross-sectionally and modulate AD pathogenesis. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy (CAA) is driven by vascular Aβ (amyloid-beta) deposition, which can be detected as reduced Aβ species in cerebrospinal fluid (CSF). 4 key findings →
Design: cross-sectional Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This study investigated whether longitudinal changes in CSF AD biomarkers were associated with 18 F-MK6240 tau PET measures in early Braak stage subregions. 4 key findings →
Design: cross-sectional Participants: 78 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Numerous imaging variables differed by clinical diagnosis, including hippocampal, amygdalar and inferior lateral ventricular volumes and entorhinal, lingual, inferior parietal and isthmus cingulate cortical thicknesses, at a false discovery rate (FDR)-corrected threshold for significance (analysis of covariance; p < 0.005). 3 key findings →
Participants: 191 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In HC and MCI subjects, FBP PET anterior and posterior cingulate and composite standard uptake value ratios correlated with CSF amyloid beta (Aβ1-42) and tau/Aβ1-42 ratios. 5 key findings →
Design: cross-sectional 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 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.
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