27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tauopathies are neurodegenerative diseases characterized by aberrant forms of tau protein accumulation leading to neuronal death in focal brain areas. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We demonstrate for the first time a link between MBI and early AD pathology in a cognitively intact elderly population, supporting the use of the MBI-C as a metric to enhance clinical trial enrolment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Determining the relative contribution of amyloid plaques and neurofibrillary tangles to brain dysfunction in Alzheimer disease is critical for therapeutic approaches, but until recently could only be assessed at autopsy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ligands targeting tau for use with positron emission tomography have rapidly been developed during the past several years, enabling the in vivo study of tau pathology in patients with Alzheimer's disease and related non-Alzheimer's disease tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Two monoclonal antibodies (mAbs), aducanumab and lecanemab, have received accelerated approval from the US FDA for initiation of treatment in early Alzheimer's disease patients who have proven β-amyloid pathology (Aβ). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activity of the glymphatic system may be evaluated with diffusion images. 2 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
Extracellular deposition of amyloid-β as neuritic plaques and intracellular accumulation of hyperphosphorylated, aggregated tau as neurofibrillary tangles are two of the characteristic hallmarks of Alzheimer's disease 1,2 . 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is an urgent need for novel therapeutic approaches for AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, several high dimensional classification methods have been proposed to automatically discriminate between patients with Alzheimer's disease (AD) or mild cognitive impairment (MCI) and elderly controls (CN) based on T1-weighted MRI. 4 key findings →
Participants: 509 Evidence: low
Full summary, score breakdown and related studies → Original source
The geometric distribution and increased burden of retinal amyloid pathology in AD, together with the feasibility to noninvasively detect discrete retinal amyloid deposits in living patients, may lead to a practical approach for large-scale AD diagnosis and monitoring. 5 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
Our data strengthens the link between retinal ganglion cell neuronal and optic nerve axonal loss with AD, and suggest that assessment of macular GC-IPL can be a test to detect neuronal injury in early AD and MCI. 4 key findings →
Participants: 123 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's participants showed significantly reduced macular VD, PD, and GC-IPL thickness compared with MCI and controls. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Tau is one of several proteins associated with frontotemporal dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To assess the ability of [18F]PI-2620 to detect regional tau burden in non-Alzheimer's disease tauopathies compared with Alzheimer's disease, patients with progressive supranuclear palsy (n = 3), corticobasal syndrome (n = 2), corticobasal degeneration (n = 1) or Alzheimer's disease (n = 8), and healthy controls (n = 7) were recruited. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Radiotracer [18F]Flortaucipir is an FDA-approved diagnostic agent for PET imaging of density and distribution of abnormal tau protein deposition (tauopathies) in Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[18F]Flortaucipir is a PET tau tracer used to visualize tau binding in Alzheimer's disease (AD) in vivo. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
APOE ε4 showed significant (P < .05) associations with tau deposition across all disease stages. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Most participants were cognitively normal (427 of 491 [87%]) and the mean age was 69.0 ± 8.8 years. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
SUVr calculated by our method and CortexID were highly correlated (R2 = 0.9657). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease-related atrophy in the posterior cingulate cortex, a key node of the default mode network, is present in the early stages of disease progression across clinical phenotypic variants of the disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
DTI revealed significant differences in white matter diffusivity between CCD and cognitively healthy aged dogs. 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
We found that patients with T2DM exhibited cognitive function declines and functional connectivity disruptions within the default mode network, left frontal parietal network, and sensorimotor network. 3 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
There was a significant association between greater Affective factor symptoms and reduced FPCN connectivity (p = 0.03). 5 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source
Regional functional connectivity (FC) of 39 patients with Alzheimer's disease (AD), 23 patients with mild cognitive impairment (MCI), and 43 healthy elderly controls was studied using resting-state functional magnetic resonance imaging (rs-fMRI). 4 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source
Preserving brain health is essential to maintaining quality of life and cognitive function with age. 1 key finding →
Evidence: low
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 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 →