31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We identified that combining plasma p-tau217 and a brief cognitive composite score was strongly related to greater risk of progression to AD dementia in MCI patients, suggesting that these measures could be key components of future prognostic algorithms for early AD. 2 key findings →
Participants: 110 Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging plasma biomarkers of Alzheimer's disease might be non-invasive tools to trace early Alzheimer's disease-related abnormalities such as the accumulation of amyloid-beta peptides, neurofibrillary tau tangles, glial activation and neurodegeneration. 4 key findings →
Design: longitudinal study Participants: 164 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Several promising plasma biomarkers for Alzheimer's disease have been recently developed, but their neuropathological correlates have not yet been fully determined. 2 key findings →
Design: longitudinal study Participants: 105 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) tau (total tau, T-tau), neurofilament light (NFL), and neurogranin (Ng) are potential biomarkers for neurodegeneration in Alzheimer's disease (AD). 3 key findings →
Design: longitudinal study Participants: 93 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Perioperative changes in plasma amyloid do not appear to be associated with postoperative delirium. 5 key findings →
Design: cohort study Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF Aβ levels are altered in a subset of patients with early PD and relate to memory impairment. 4 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our data suggest that measuring blood biomarkers related to AD pathology and neurodegeneration from DPS venous extends the utility of blood-based biomarkers to remote settings with simplified sampling conditions, storage, and logistics. 4 key findings →
Participants: 154 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Comparable diagnostic performances and strong correlations between serum versus plasma pairs suggest that p-tau analyses can be expanded to research cohorts and hospital systems that prefer serum to other blood matrices. 5 key findings →
Participants: 115 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 demonstrated better performance in the identification of AD pathology and clinical phenotypes in comparison with other variants of p-tau in a memory clinic cohort. 5 key findings →
Participants: 114 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Failures in Alzheimer's disease (AD) drug trials highlight the need to further explore disease mechanisms and alterations of biomarkers during the development of AD. 3 key findings →
Design: cross-sectional Participants: 377 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma tau phosphorylated at threonine 181 (p-tau181) predicts Alzheimer's disease (AD) pathology with high accuracy in the general population. 2 key findings →
Participants: 366 Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormal plasma Aβ42/40 ratio identified older adult groups with lower memory scores, higher dementia risks, and higher ADRD biomarker levels, with potential implications for population screening. 2 key findings →
Participants: 847 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These in vivo data support the role of Aβ pathology in the etiology and highlight the potential utility of CSF Aβ42 as an early prognostic biomarker of dementia associated with PD. 3 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Beta-amyloid (Aβ 1-42 ) triggers the phosphorylation of tau protein in Alzheimer's disease (AD), but the relationship between phosphorylated tau (p-tau) and Aβ 1-42 in the blood is not elucidated. 4 key findings →
Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source
Creatinine and BMI are related to certain plasma biomarkers levels, but they do not have clinically relevant confounding effects for the vast majority of individuals. 1 key finding →
Participants: 748 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers related to amyloid, tau, and neurodegeneration (ATN) show great promise for identifying these pathological features of Alzheimer's Disease (AD) as shown by recent clinical studies and selected autopsy studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A combination of plasma Aβ42/Aβ40 and p-tau217 discriminated Aβ status with relatively high accuracy, whereas p-tau217 showed strongest associations with Aβ pathology in MCI but not in CU. 1 key finding →
Participants: 591 Evidence: low
Full summary, score breakdown and related studies → Original source
Up to four freeze-thaw cycles do not influence single molecule array blood biomarkers of neurofilament light chain, total tau, or Aβ 42 , with at most minor reductions in Aβ 40 . 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
This study identified the plasma biomarker analytes and assays that most accurately classified amyloid pathology and other AD-related outcomes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
P-tau isoforms can be measured robustly by several novel high-sensitive Simoa assays. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
HIGHLIGHTS: Different plasma phosphorylated tau (p-tau) species reflect different pathological processes of Alzheimer's disease (AD), with p-tau231 showing the greatest association with the earliest increases in brain amyloid beta (Aβ) accumulation, while p-tau217 shows greater association with both brain Aβ and early tau pathology, and other p-tau and tau fragment species show greater association with later stages of brain tau pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that although plasma and CSF neurogranin may reflect the volume of acute cerebral ischemia, this synaptic protein is less likely to be a potential AIS biomarker. 4 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we determined the diagnostic accuracy of cerebrospinal fluid (CSF) biomarkers to predict development of Alzheimer's disease (AD) within five years in patients with mild cognitive impairment (MCI). 1 key finding →
Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source
IR among asymptomatic APOEɛ4 carriers was associated with higher P-Tau181 and T-Tau in late-middle age. 5 key findings →
Participants: 113 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma NfL indicates neurodegeneration while plasma p-tau181 levels can serve as a biomarker of cerebral AD pathology and cognitive decline. 2 key findings →
Evidence: low
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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