28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Growing evidence indicates that apolipoprotein E (ApoE) is one of the most important candidate genes for influencing the development of hemodialysis (HD). 3 key findings →
Design: case-control study Participants: 485 Evidence: moderate
Full summary, score breakdown and related studies → Original source
After analytical validation, the diagnostic performance of these biomarkers was evaluated in CSF and compared with the Innotest total tau (and as proof of concept, with N-p-tau181 and N-p-tau217) in three clinical cohorts (n = 342 total). 5 key findings →
Participants: 342 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain degeneration in patients with Alzheimer's disease (AD) results from the accumulation of pathological amyloid- (Aβ) plaques and tau protein tangles, leading to altered plasma levels of biomarkers. 5 key findings →
Design: cross-sectional Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Little is known whether cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) can predict both memory decline and associated longitudinal medial temporal lobe (MTL) gray matter (GM) reductions in cognitively healthy individuals. 2 key findings →
Design: longitudinal study Participants: 57 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our findings support an association of APOE ɛ4 and p-tau181 with preclinical AD and hippocampus functioning. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Longitudinal OEF change in older adults is primarily related to vascular pathology. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyloid, tau, neurodegeneration and neuroinflammation plasma biomarkers are modified in DLB, albeit with moderate diagnosis performance. 2 key findings →
Participants: 104 Evidence: low
Full summary, score breakdown and related studies → Original source
Slow paced breathing via heart rate variability (HRV) biofeedback stimulates vagus-nerve pathways that counter noradrenergic stress and arousal pathways that can influence production and clearance of Alzheimer's disease (AD)-related proteins. 2 key findings →
Participants: 108 Evidence: high
Full summary, score breakdown and related studies → Original source
Unlike previous research that used traditional immunoassay, recent studies that measured plasma Aβ42/40 using fully automated platforms reported promising results. 3 key findings →
Participants: 174 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma tau phosphorylated at threonine 181 (p-tau181) and 217 (p-tau217) have demonstrated high accuracy for Alzheimer's disease (AD) diagnosis, defined by CSF/PET amyloid beta (Aβ) positivity, but most studies have been performed in research cohorts, limiting their generalizability. 3 key findings →
Participants: 468 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma proteins improved classification accuracy of AD pathology in cognitively-impaired older adults and appeared representative of amyloid pathology. 1 key finding →
Design: cross-sectional Participants: 72 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our multimarker blood test interpretation tool is ready for testing in real-world clinical dementia settings. 4 key findings →
Participants: 1,199 Evidence: low
Full summary, score breakdown and related studies → Original source
CSF biomarkers of angiogenesis are increased in PD, and they are associated with gait difficulties, BBB dysfunction, WMLs, and CMB. 5 key findings →
Design: cross-sectional Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
Lumipulse plasma Aβ 42 /Aβ 40 is a scalable assay for detection of cerebral Aβ and prediction of risk for cognitive decline across the AD continuum. 2 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum Abeta40/42 ratio was significantly higher in MDD patients than in controls, and this difference was seen for both elderly and young subjects. 5 key findings →
Design: cohort study Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Levels of plasma Aβ42 and Aβ42/Aβ40 ratio were elevated in patients with possible cognitive impairment, indicating that plasma Aβ42 and Aβ42/Aβ40 ratio increases may be more pronounced in early stage of cognitive impairment. 2 key findings →
Design: cross-sectional Participants: 1,314 Evidence: low
Full summary, score breakdown and related studies → Original source
Exposure to environmental chemicals such as lead (Pb) during vulnerable developmental periods can result in adverse health outcomes later in life. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Including apolipoprotein E-ε4 (APOE-ε4) status and older age into consideration may increase the accuracy of plasma Aβ 42 /Aβ 40 detecting Aβ+ individuals, but the rationale behind this remains to be fully understood. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
These data suggest that IL6 trans-signaling and the inheritance of the IL6R Ala 358 variant are related to reduced cognition and greater levels of biomarkers for AD disease pathology. 4 key findings →
Design: cross-sectional Participants: 120 Evidence: low
Full summary, score breakdown and related studies → Original source
We identified a series of transmembrane proteins, proteins associated with or anchored to the plasma membrane, and proteins involved in or connected to synaptic vesicle transport to be associated with CSF biomarkers of amyloid and tau pathology in AD. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent large scale CSF proteomic studies revealed several new AD candidate biomarkers related to metabolic pathways. 5 key findings →
Participants: 19 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There are biologically meaningful Aβ-downstream effects in individuals with a low burden of Aβ pathology, while structural and functional changes are still subtle or absent. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Different stages of Parkinson's disease (PD) are defined by clinical criteria, while late-stage PD is marked by the onset of morbidity milestones and rapid clinical deterioration. 3 key findings →
Participants: 118 Evidence: low
Full summary, score breakdown and related studies → Original source
Using blood samples from the publicly available ADNI research cohort (191 people with mild cognitive impairment or dementia), this study found the PrecivityAD2 blood test agreed with amyloid PET scans about 91% of the time. 3 key findings →
Design: cross-sectional Participants: 191 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Genetic risk for AD does not modify the association between hypertension and dementia. 4 key findings →
Design: cohort Participants: 11,597 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →