Hippocampal volume change over time, measured with MRI, has huge potential as a marker for Alzheimer's disease. 1 key finding →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Hippocampal volume change over time, measured with MRI, has huge potential as a marker for Alzheimer's disease. 1 key finding →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source
Major imaging biomarkers of Alzheimer's disease include amyloid deposition [imaged with [(11)C]Pittsburgh compound B (PiB) PET], altered glucose metabolism (imaged with [(18)F]fluro-deoxyglucose PET), and structural atrophy (imaged by MRI). 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
We implemented least absolute shrinkage and selection operator (LASSO) regression to evaluate gene effects in genome-wide association studies (GWAS) of brain images, using an MRI-derived temporal lobe volume measure from 729 subjects scanned as part of the Alzheimer's Disease Neuroimaging Initiative (ADNI). 3 key findings →
Participants: 729 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We found that ML-PRS approaches improved upon standard PRS for prediction of AD endophenotypes, partly related to improved accounting for nonlinear effects of genetic susceptibility alleles. 3 key findings →
Participants: 1,791 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Suspected non-Alzheimer disease pathophysiology (SNAP) is a biomarker-based concept that applies to individuals with normal levels of amyloid-β biomarkers in the brain, but in whom biomarkers of neurodegeneration are abnormal. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The regions of loss observed in subjects with amnestic mild cognitive impairment (aMCI) who progressed to Alzheimer disease (AD) within 18 months of the MRI are typical of subjects with AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
55 of the 152 (36.2 %) aMCI subjects progressed to AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Brain imaging with diffusion-weighted MRI (dMRI) is sensitive to microstructural white matter (WM) changes associated with brain aging and neurodegeneration. 4 key findings →
Participants: 317 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The APOE*E4 genotype status appears to have a greater deleterious effect on gross hippocampal pathology and memory performance in women than in men. 4 key findings →
Participants: 193 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
White matter hyperintensity volume predicts 1-year cognitive decline in a relatively healthy convenience sample that was similar to clinical trial samples, and therefore should be considered as a covariate of interest at baseline and longitudinally in future AD treatment trials. 3 key findings →
Participants: 804 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hippocampal ADC was significantly different between control subjects and MCI patients, many of whom likely have preclinical Alzheimer disease. 2 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We recently demonstrated that the frequencies of biomarker groups defined by the presence or absence of both amyloidosis (A+) and neurodegeneration (N+) changed dramatically by age in cognitively non-impaired subjects. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
ADNI has had a profound impact in improving clinical trials for AD. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this cross-sectional study, we found an association between Aβ brain burden measured in vivo and DBP and cortisol, indicating a possible link between these CVRF and Aβ burden measured by PiB-PET. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Of the 296 initially normal subjects, 31 (10%) progressed to a diagnosis of mild cognitive impairment (MCI) or dementia (27 amnestic MCI, 2 nonamnestic MCI, and 2 non-AD dementias) within 1 year. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
MRI research examining structural brain atrophy in Alzheimer's disease (AD) generally focuses on medial temporal and cortical structures, but amyloid and tau deposits also accumulate in the caudate. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As preclinical Alzheimer's disease becomes a target for therapeutic intervention, the overlap between imaging abnormalities associated with typical ageing and those associated with Alzheimer's disease needs to be recognised. 4 key findings →
Participants: 985 Evidence: low
Full summary, score breakdown and related studies → Original source
The National Institute on Aging and the Alzheimer's Association convened three separate work groups in 2011 and single work groups in 2012 and 2018 to create recommendations for the diagnosis and characterization of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In region-of-interest (ROI) analyses, we found modest but statistically significant declines in FDG ratio in most cortical and subcortical regions as a function of age. 4 key findings →
Participants: 806 Evidence: low
Full summary, score breakdown and related studies → Original source
Prior MR imaging studies, primarily at 1.5T, established hippocampal atrophy as a biomarker for Alzheimer disease. 3T MR imaging offers a higher contrast and signal-to-noise ratio, yet distortions and intensity uniformity are harder to control. 4 key findings →
Participants: 166 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Despite the theoretical rationale for the superiority of entorhinal measurements in early AD, the authors found MRI measurements of the hippocampus and entorhinal cortex were approximately equivalent at intergroup discrimination. 2 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
A variety of anatomic and functional neuroimaging findings are associated with Alzheimer's disease (AD). 4 key findings →
Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results confirm plasma β-amyloid 42 /β-amyloid 40 as a robust biomarker of brain β-amyloid-positivity (area under curve, 0.80-0.87). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The current study tested the accuracy of primary MRI and cerebrospinal fluid (CSF) biomarker candidates and neuropsychological tests for predicting the conversion from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia. 1 key finding →
Participants: 81 Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitively normal persons with brain injury biomarker abnormalities, with or without abnormal levels of β-amyloid, were indistinguishable on a variety of imaging markers, clinical features, and risk factors. 2 key findings →
Design: cross-sectional 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events