28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The levels of α-synuclein oligomers and oligomers/total-α-synuclein ratio in CSF were higher in the PD group (n = 32; p < 0.0001, Mann-Whitney U test) compared to the control group (n = 28). 5 key findings →
Design: cross-sectional Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
Social cognitive impairments are consistently reported in schizophrenia and are associated with functional outcome. 3 key findings →
Design: cross-sectional Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A large body of evidence suggests that not only cerebral but also systemic oxidative stress (OxS) might be involved in the pathogenesis of late onset Alzheimer’s disease (LOAD) and vascular dementia (VAD), as well as of the prodromal phase of dementia, the so-called mild cognitive impairment (MCI). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The PrecivityAD2 blood test showed strong clinical validity, with excellent agreement with brain amyloidosis by PET. 1 key finding →
Participants: 583 Evidence: low
Full summary, score breakdown and related studies → Original source
We found strong evidence that plasma p-tau 181 is elevated in ALS and may be a novel marker specific to LMN dysfunction. 4 key findings →
Participants: 130 Evidence: low
Full summary, score breakdown and related studies → Original source
A growing literature suggests that plasma levels of tau phosphorylated at amino acid 217 (pTau217) performs similarly to cerebrospinal fluid (CSF) biomarkers and PET imaging to detect amyloid pathology and to provide diagnostic and prognostic information in Alzheimer's disease (AD), but a significant limiting factor thus far has been a lack of widely available immunoassays. 2 key findings →
Participants: 131 Evidence: low
Full summary, score breakdown and related studies → Original source
Breakdown of the neurovascular unit is associated with blood-brain barrier (BBB) leakiness contributing to cognitive decline and disease pathology in the early stages of Alzheimer's disease (AD). 3 key findings →
Participants: 121 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood phosphorylated tau (p-tau) biomarkers, including p-tau217, show high associations with Alzheimer's disease (AD) neuropathologic change and clinical stage. 1 key finding →
Participants: 388 Evidence: low
Full summary, score breakdown and related studies → Original source
The identified cutoffs and probability-based models represent a significant step toward plasma AD molecular diagnosis. 2 key findings →
Participants: 450 Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies have demonstrated increased tau plasma levels in patients with Alzheimer's disease (AD) and mild cognitive impairment (MCI) due to AD. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The immune system substantially influences age-related cognitive decline and Alzheimer's disease (AD) progression, affected by genetic and environmental factors. 3 key findings →
Participants: 298 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma biomarkers differed across diagnostic groups (DEM > MCI > CU), were altered in Aβ-PET-positive individuals, and were associated with poorer brain health and kidney function. 2 key findings →
Participants: 299 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers such as tau phosphorylated at threonine 181 (phosphorylated-tau181) represent an accessible, cost-effective and scalable approach for the in vivo detection of Alzheimer's disease pathophysiology. 5 key findings →
Participants: 103 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 shows excellent results for detecting amyloid pathology at brain level in a clinical setting with an AUC of 0.95. 2 key findings →
Participants: 493 Evidence: low
Full summary, score breakdown and related studies → Original source
Severity of cognitive impairment and race both influence plasma p-Tau 217 levels beyond race-associated differences in CSF p-Tau 181 . 4 key findings →
Participants: 113 Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings highlight that plasma p-tau181, alone or combined with NfL, contributes to identifying high-risk AD populations. 3 key findings →
Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers may differentiate non-AD-related versus AD-related cognitive deficits. 5 key findings →
Participants: 648 Evidence: low
Full summary, score breakdown and related studies → Original source
Combining co-pathology markers may identify individuals with a high risk of cognitive decline. 2 key findings →
Participants: 262 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by brain protein depositions, impaired synaptic transmission, and progressive cognitive decline. 2 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
In the tea-consuming group, the MoCA scores ( P = 0.000), Hopkins Verbal Learning Test (HVLT) immediate recall ( P = 0.012) and delayed recall ( P = 0.013) were significantly higher while Trail Making Test-B ( P = 0.005) and Victoria Stroop test interference ( P = 0.000) were lower. 5 key findings →
Participants: 264 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) biomarkers are essential for the accurate diagnosis of Alzheimer's disease (AD), yet their measurement levels vary widely across centers and regions, leaving no uniform cutoff values to date. 5 key findings →
Participants: 64 Evidence: moderate
Full summary, score breakdown and related studies → Original source
NfL and p/t-tau similarly discriminated FTD from controls, but not between clinical subtypes, apart from FTD-MND. 2 key findings →
Participants: 361 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum GFAP is increased in FTLD, correlates with cognition and GABAergic deficits, and thus shows promise as a biomarker of disease severity in FTLD. 3 key findings →
Design: cross-sectional Participants: 406 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The study shows individuals with a high APS are more likely than those with a low APS to have abnormal amounts of amyloid plaques and be on an amyloid accumulation trajectory, a dynamic and evolving process characteristic of progressive AD pathology. 1 key finding →
Participants: 13 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We examined the effects of a dihydropyridine calcium channel blocker nilvadipine with anti-inflammatory properties on cognition and cerebrospinal fluid (CSF) biomarkers by baseline Alzheimer's disease (AD) severity. 4 key findings →
Participants: 497 Evidence: high
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 →