27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Highly sensitive and specific plasma biomarkers for Alzheimer's disease (AD) have the potential to improve diagnostic accuracy in the clinic and facilitate research studies including enrollment in prevention and treatment trials. 1 key finding →
Participants: 36 Evidence: moderate
Full summary, score breakdown and related studies → Original source
β-blockers that easily cross the blood-brain barrier (BBB) seem to diminish the risk of Alzheimer's disease (AD), hypothetically facilitating waste clearance. 3 key findings →
Participants: 216 Evidence: low
Full summary, score breakdown and related studies → Original source
We assessed cerebrospinal fluid (CSF) levels of tau and other biomarkers of neurodegenerative disease. 4 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Numerous imaging variables differed by clinical diagnosis, including hippocampal, amygdalar and inferior lateral ventricular volumes and entorhinal, lingual, inferior parietal and isthmus cingulate cortical thicknesses, at a false discovery rate (FDR)-corrected threshold for significance (analysis of covariance; p < 0.005). 3 key findings →
Participants: 191 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration, the neuropathological substrate of frontotemporal dementia (FTD), is characterized by the deposition of protein aggregates, including tau. 4 key findings →
Participants: 99 Evidence: low
Full summary, score breakdown and related studies → Original source
In HC and MCI subjects, FBP PET anterior and posterior cingulate and composite standard uptake value ratios correlated with CSF amyloid beta (Aβ1-42) and tau/Aβ1-42 ratios. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
In regression analyses across the whole study sample adjusted for age, sex, and diagnostic group, there was no relationship between HbA1c or fasting glucose and CSF tau, p-tau 182, or Abeta42 levels. 3 key findings →
Design: cross-sectional Participants: 91 Evidence: low
Full summary, score breakdown and related studies → Original source
At genera and species levels, higher subgingival periodontal dysbiosis was associated with reduced CSF amyloid beta (Aβ)42 (P = 0.02 and 0.01) but not with P-tau. 3 key findings →
Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source
We included 201 individuals (mean age 73.5 years, mean BMI 27.4 kg/m2). 4 key findings →
Participants: 201 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 96 proteins were decreased in MCI-SNAP compared to CN and MCI-AD. 5 key findings →
Participants: 96 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebral microbleeds (CMBs) are hypothesised to have an important yet unknown role in the dementia disease pathology. 4 key findings →
Participants: 1,039 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease Neuroimaging Initiative database. 4 key findings →
Participants: 57 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid angiopathy is caused by deposition of the amyloid beta protein in the cerebral vasculature. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients with autopsy-confirmed LBD (n = 24) and autopsy-confirmed Alzheimer disease (AD) (n = 23) and cognitively normal (n = 36) controls were studied. 4 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To better understand how sleep/wake dysregulation affects Alzheimer's disease (AD), we compared the cerebrospinal fluid (CSF) orexin and histamine/tele-methylhistamine (HA/t-MHA) levels of 82 patients (41 probable-AD-high level of evidence, 41 mild cognitive impairment MCI-due-to-AD), 24 other neurologic disorders (OND) and 24 controls. 4 key findings →
Participants: 82 Evidence: low
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Niemann-Pick disease type C (NPC) is an inherited disorder characterized by intracellular accumulation of lipids such as cholesterol and glycosphingolipids in endosomes and lysosomes. 4 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Although typical forms of Alzheimer disease (AD) and Creutzfeldt-Jakob disease (CJD) are clinically distinguishable, atypical AD phenotypes may pose a diagnostic challenge. 4 key findings →
Participants: 82 Evidence: moderate
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This prospective observational study included 22 patients with PCA who underwent CSF biomarker analysis of total tau (t-tau), phosphorylated tau on amino acid 181 (p-tau181), and amyloid β (Aβ(42)). 4 key findings →
Participants: 22 Evidence: low
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We developed and validated a novel Simoa immunoassay to detect p-tau T217 in CSF. 4 key findings →
Participants: 77 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The ability of Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers (amyloid β peptide 1-42, total tau, and phosphorylated tau) to discriminate AD from related disorders is limited. 4 key findings →
Participants: 367 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Irisin, released by muscles during exercise, was recently identified as a neuroprotective factor in mouse models of Alzheimer disease (AD). 4 key findings →
Participants: 82 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The current study examined the interactive effect of type 2 diabetes and Alzheimer disease (AD) risk factors on the rate of functional decline in cognitively normal participants from the Alzheimer's Disease Neuroimaging Initiative. 4 key findings →
Design: longitudinal study Participants: 69 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Isoprostanes and prostaglandins are biomarkers for oxidative stress and inflammation. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The apolipoprotein E (APOE)ε4 allele is the strongest genetic risk factor for late-onset AD and is associated with aberrant cerebrospinal fluid levels (CSF) of total tau (t-tau), phosphorylated tau (p-tau), and amyloid-β (Aβ). 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
It is unknown whether multidomain interventions, which might preserve late-life cognition, affect Alzheimer's disease pathology. 4 key findings →
Participants: 527 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →