28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In particular, systemic inflammation, vascular inflammation, and altered endothelial function may play roles in domain-specific cognitive decline of nondemented individuals. 1 key finding →
Design: randomized controlled trial Participants: 1,159 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood biomarkers indicative of Alzheimer's disease (AD) pathology are altered in both preclinical and symptomatic stages of the disease.
Full summary, score breakdown and related studies → Original source Free full text
Blood biomarkers indicating elevated amyloid-β (Aβ) pathology in preclinical Alzheimer's disease are needed to facilitate the initial screening process of participants in disease-modifying trials. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
A combination of plasma p-tau181, NfL, and GFAP, but not Aβ 1-42/1-40 , might be useful to discriminate AD, FTD, and DLB. 1 key finding →
Participants: 160 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We detected an increased concordance in the visual and quantitative (standardized uptake value ratio (SUVR) and total volume of distribution (VT)) [18F]AV45 PET measures when the CSF Aβ1-42/Aβ1-40 was applied compared to Aβ1-42 alone. 2 key findings →
Design: longitudinal study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline NfL was elevated in symptomatic carriers (median 52 pg/mL [IQR 24-69]) compared with presymptomatic carriers (9 pg/mL [6-13]; p<0·0001) and non-carriers (8 pg/mL [6-11]; p<0·0001), and was higher in converters than in non-converting carriers (19 pg/mL [17-28] vs 8 pg/mL [6-11]; p=0·0007; adjusted for age). 4 key findings →
Design: cohort study Participants: 59 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Tau is an axonal microtubule-binding protein. 5 key findings →
Design: cross-sectional Participants: 133 Evidence: moderate
Full summary, score breakdown and related studies → Original source
PF and BF were significantly associated with increased likelihoods of dementia, Alzheimer's disease (AD), vascular dementia (VaD), and MCI. 5 key findings →
Design: cross-sectional Participants: 5,149 Evidence: low
Full summary, score breakdown and related studies → Original source
Higher plasma p-tau levels were associated with worse cognition at baseline and over time, with the strongest effect observed with p-tau217 in cognitively impaired individuals (β = -0.49, p < 0.001). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
T-tau, NfL, GFAP, and YKL-40 discriminated between diagnostic groups (receiver operating curve: 0.647-0.873). 5 key findings →
Participants: 1,193 Evidence: moderate
Full summary, score breakdown and related studies → Original source
After adjusting for age, plasma NfL level was higher in subjects with DAT (65.98±84.96 pg/mL), compared to in subjects with SCD (16.90±2.54 pg/mL) or MCI (25.53±10.42 pg/mL, p=0.004). 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Of 349 participants with available plasma data, 234 met inclusion criteria (31 controls, 141 in the training sample, and 62 in the validation sample). 5 key findings →
Design: cross-sectional Participants: 46 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma GFAP discriminated AD dementia from normal cognition (adjusted mean difference = 0.90 standard deviation [SD]) and mild cognitive impairment (adjusted mean difference = 0.72 SD), and demonstrated superior discrimination compared to alternative plasma biomarkers. 4 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
Full summary, score breakdown and related studies → Original source
NfL, Aβ40, Aβ42, GFAP, and p-tau181 were detected in all AH samples by Simoa platform. 5 key findings →
Design: cohort study Participants: 55 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Delirium is associated with cognitive decline and subsequent dementia, and rises in plasma total tau (tTau) and neurofilament light (NfL), providing links to Amyloid-Tau-Neurodegeneration (ATN) pathophysiology. 4 key findings →
Design: cohort study Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Pathophysiological substrate(s) and progression of Parkinson's disease (PD) with mild cognitive impairment (PD-MCI) are still matter of debate. 2 key findings →
Design: longitudinal study Participants: 48 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Participants were classified as hyposecretors (n = 22, median Aβ40 5,870.500 pg/mL, interquartile range [IQR] 1,431), normosecretors (n = 47, median Aβ40 10,817 pg/mL, IQR 3,622), and hypersecretors (n = 7, 19,767 pg/mL, IQR 3,088). 5 key findings →
Design: retrospective cohort Participants: 22 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Family history (FH) of late-onset Alzheimer's disease (AD) is associated with changes in several cerebrospinal fluid (CSF) biomarkers in cognitively normal individuals. 2 key findings →
Design: longitudinal study Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The Panama Aging Research Initiative is a cohort study of 423 adults aged ≥65 years recruited from an outpatient geriatric department of Panama's largest public hospital, the Social Security Fund's Dr Arnulfo Arias Madrid Hospital Complex (Complejo Hospitalario Dr Arnulfo Arias Madrid de la Caja de Seguro Social). 5 key findings →
Design: cohort study Participants: 423 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In subjects with biomarker-confirmed Alzheimer's pathology, high CSF ferritin (>6.2 ng/mL) was associated with accelerated depreciation of CSF Aβ1-42 (reporting increased plaque formation; p=0.0001). 5 key findings →
Design: longitudinal study Participants: 296 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
Identifying which neuropsychological measures detect early cognitive changes associated with Alzheimer disease (AD), brain pathology would be helpful clinically for the diagnosis of early AD and for the design of clinical trials. 3 key findings →
Design: longitudinal study Participants: 233 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Intra- and inter-laboratory variability of cerebrospinal fluid (CSF) biomarker analyses remains an important issue. 1 key finding →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Carriers had lower LAS-FNAME performance (P < 0.001) and higher p-tau217 (P < 0.001), NfL (P = 0.013), and GFAP (P < 0.001) levels than non-carriers. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF was αSyn-SAA positive (αSyn+) in 36/80 AD patients (45%) and in 2/28 controls (7.1%). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
10 of the 3,322 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 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 →