28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings suggest that promoting CVH in older adults may help alleviate the burden of neurodegenerative diseases, particularly among Black adults, who are known to experience a higher prevalence of cardiovascular disease. 5 key findings →
Design: cohort study Participants: 1,018 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
N-p-tau217 and N-p-tau181 could improve diagnostic accuracy in prodromal-AD and clinical trial recruitment as both identify Aβ pathophysiology and differentiate early MCI-AD better than Mid-p-tau181. 2 key findings →
Participants: 503 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma P-tau181/Aβ42 ratio may be a noninvasive means of identifying AD with elevated brain amyloid in populations with concomitant CeVD. 3 key findings →
Participants: 43 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Both plasma p-tau217 assays were strongly associated with amyloid and tau PET. 1 key finding →
Participants: 294 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma amyloid-β (Aβ)42, phosphorylated tau (p-tau)181, and neurofilament light chain (NfL) are promising biomarkers of Alzheimer's disease (AD). 2 key findings →
Participants: 126 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma pTau217 had a high correlation with both Aβ Centiloid (r = 0.76) and tau SUVR meta-temporal (r = 0.78). 2 key findings →
Participants: 388 Evidence: low
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
P-tau and NfL behave differently within the same individuals over time and may therefore offer complementary diagnostic information. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
A panel of nine CSF biomarkers was able to differentiate APS from patients with PD and dementia. 2 key findings →
Design: prospective cohort Participants: 31 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two related currently incurable neurodegenerative diseases. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Rationale and objectives Mild cognitive impairment has been regarded as a pre-Alzheimer condition, but some patients do not develop dementia. 3 key findings →
Design: longitudinal study Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau is a stronger indicator of a temporally linked response to elevated brain Aβ than of tau pathology. 4 key findings →
Participants: 1,408 Evidence: low
Full summary, score breakdown and related studies → Original source
We found a strong, positive correlation between all the measurements. 5 key findings →
Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 239 participants underwent blood draw and Aβ-PET (age 70.8 ± 7.8, 55.2% female, education 15.6 ± 3.4 years, 48.9% Hispanic/Latino, 94.9% white). 5 key findings →
Participants: 239 Evidence: low
Full summary, score breakdown and related studies → Original source
Greater multimorbidity burden was associated with worse cognition and biomarkers of AD (PET amyloid standardized uptake value ratios and positivity, p-tau181, and p-tau217), neurodegeneration (neurofilament light, total tau, cortical thickness, and hippocampal volume), and SVD (white matter hyperintensity volume and presence of lacune and cerebral microbleeds). 3 key findings →
Participants: 3,808 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers have emerged as promising less invasive alternatives for Alzheimer's disease (AD) detection. 2 key findings →
Participants: 53 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent advances in blood-based biomarkers of Alzheimer's Disease (AD) show great promise for clinical applications, offering a less invasive alternative to current cerebrospinal fluid (CSF) measures. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We constructed a panel combining plasma NfL and GFAP with known AD risk factors (Combination panel: age+sex+APOE4+GFAP+NfL). 5 key findings →
Design: cross-sectional Participants: 63 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma GFAP levels were significantly (all p < 0.001) elevated in bvFTD (n = 22, mean (M) = 273 pg/mL) compared to BPAD (n = 121, M = 96 pg/mL), MDD (n = 42, M = 105 pg/mL), TRS (n = 82, M = 67.9 pg/mL), and HC (n = 120, M = 76.8 pg/mL). 5 key findings →
Participants: 22 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma neurofilament light (NfL) protein is a promising non-invasive biomarker for detecting neuronal damage in Alzheimer's disease (AD). 5 key findings →
Participants: 860 Evidence: moderate
Full summary, score breakdown and related studies → Original source
BackgroundHearing loss is one of the most prominent modifiable risk factors for dementia, accounting for one of the largest population-attributable risk among midlife exposures according to the Lancet Commission on Dementia. 5 key findings →
Design: cross-sectional Participants: 373 Evidence: low
Full summary, score breakdown and related studies → Original source
Both atrophy (AUC = 0.87, 95% confidence interval [95% CI: 0.79 to 0.94]) and NfL (AUC = 0.89, 95% CI: 0.81 to 0.96) showed significant predictive ability, which improved when combined (AUC = 0.93, 95% CI: 0.87 to 0.99). 5 key findings →
Participants: 55 Evidence: low
Full summary, score breakdown and related studies → Original source
CSF total aSyn was decreased. NfL, pNfH, UCHL-1, GFAP, S100B, and sTREM-2 were increased in patients with neurodegenerative disease versus HC (P < 0.05). 5 key findings →
Participants: 151 Evidence: moderate
Full summary, score breakdown and related studies → Original source
53% of participants were CMV seropositive. 5 key findings →
Design: cross-sectional Participants: 303 Evidence: low
Full summary, score breakdown and related studies → Original source
BackgroundRetinal thickness has been associated with neurocognitive conditions such as Alzheimer's disease (AD).ObjectiveRetinal cell layer thickness was evaluated for associations with neurodegenerative protein biomarkers glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) in plasma, vitreous humor, and aqueous humor. 5 key findings →
Design: cross-sectional Participants: 50 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →