30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
PD patients who develop poor outcomes show lower DTI-ALPS, potentially reflecting impaired glymphatic clearance. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
During follow-up, 57 (42%) patients with MCI developed Alzheimer's disease, 21 (15%) developed other forms of dementia, and 56 (41%) remained cognitively stable for 5.2 years (range 4.0-6.8). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
PET, CSF and plasma biomarkers of tau pathology may be differentially associated with Alzheimer's disease (AD)-related demographic, cognitive, genetic and neuroimaging markers. 3 key findings →
Participants: 400 Evidence: low
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Widespread implementation of cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) in clinical settings requires improved accuracy for diagnosis of prodromal disease and for distinguishing AD from non-AD dementias. 4 key findings →
Participants: 338 Evidence: moderate
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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
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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
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
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
Blood biomarkers are rapidly becoming established for Alzheimer's Disease (AD) diagnosis. 2 key findings →
Participants: 174 Evidence: low
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The proposed novel, pragmatic method to determine CSF biomarker cutoffs for AD does not require assessment of other biomarkers or assumptions concerning the clinical diagnosis of patients. 1 key finding →
Participants: 497 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid and positron emission tomography amyloid-β were measured at baseline in 769 persons [161 healthy controls, 68 subjective memory complaints, 419 mild cognitive impairment and 121 Alzheimer's disease dementia, mean age 72 years (standard deviation 7 years), 47% females] and used to predict diagnosis, APOE ε4 carriage status, cerebral blood flow, cerebrospinal fluid total-tau and phosphorylated-tau levels (cross-sectionally); and hippocampal volume, fluorodeoxyglucose positron emission tomography results and Alzheimer's Disease Assessment Scale-cognitive subscale scores (longitudinally). 2 key findings →
Participants: 769 Evidence: low
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The cerebrospinal fluid (CSF) biochemical markers (biomarkers) Amyloidβ 42 (Aβ 42 ), total Tau (T-tau) and Tau phosphorylated at threonine 181 (P-tau 181 ) have proven diagnostic accuracy for mild cognitive impairment and dementia due to Alzheimer's Disease (AD). 5 key findings →
Evidence: low
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Intense multidisciplinary research has provided detailed knowledge of the molecular pathogenesis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Insulin, insulin-like growth factors (IGF) and their receptors are highly expressed in the adult hippocampus. 4 key findings →
Design: longitudinal study Evidence: moderate
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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
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
This study estimated the utilization and lifetime costs of formal care for AD dementia using longitudinal register data. 4 key findings →
Design: cohort Participants: 20,366 Evidence: high
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The diagnostic guidelines of Alzheimer's disease (AD) have recently been updated to include brain imaging and cerebrospinal fluid (CSF) biomarkers, with the aim of increasing the certainty of whether a patient has an ongoing AD neuropathologic process or not. 3 key findings →
Design: cross-sectional Evidence: moderate
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Early detection of prodromal Alzheimer disease (AD) is important because new disease-modifying therapies are most likely to be effective when initiated during the early stages of disease. 4 key findings →
Participants: 137 Evidence: low
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Bipolar disorder is a psychiatric disorder characterized by recurrent episodes of mania/hypomania and depression. 4 key findings →
Evidence: low
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Two genetic variants in strong linkage disequilibrium (rs9536314 and rs9527025) in the Klotho (KL) gene, encoding a transmembrane protein, implicated in longevity and associated with brain resilience during normal aging, were recently shown to be associated with Alzheimer disease (AD) risk in cognitively normal participants who are APOE ε4 carriers. 4 key findings →
Participants: 5,541 Evidence: low
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These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
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A subgroup of patients with Alzheimer disease with extreme levels of CSF biomarkers exhibits worse clinical outcomes over time, including faster progression of cognitive deficits, no response to ChEI treatment, and a higher mortality. 1 key finding →
Participants: 151 Evidence: low
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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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →