Twenty-one patients showed FDG hypometabolism; the remaining 3 did not. 1 key finding →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Twenty-one patients showed FDG hypometabolism; the remaining 3 did not. 1 key finding →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cortical thickness from MRI helped predict conversion from mild cognitive impairment to dementia in Parkinson disease at an individual level, with improved performance when integrated with clinical variables. © RSNA, 2021 Online supplemental material is available for this article. 2 key findings →
Participants: 75 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The experimental results demonstrate that the SVM with RBF achieved an encouraging performance with sensitivity (SEN), specificity (SPE), and accuracy (ACC) values of 82.65%, 87.17%, and 84.35%, respectively (AUC = 0.861, 95% CI = 0.820-0.902), for the differential diagnosis between VaD and AD. 2 key findings →
Participants: 93 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The patterns of FDG decline are distinct in these 2 genetically determined forms of AD. 1 key finding →
Design: cross-sectional Participants: 76 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We investigated the changes of sulcal shape (average mean curvature in folded regions and sulcal depth) in mild cognitive impairment (MCI) and Alzheimer's disease (AD) using quantitative surface-based methods in a large sample of magnetic resonance imaging data. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Arterial spin labeling (ASL) magnetic resonance imaging uses arterial blood water as an endogenous tracer to measure cerebral blood flow (CBF). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid imaging represents a major advance in neuroscience, enabling the detection and quantification of pathologic protein aggregations in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent genetic studies have provided overwhelming evidence of the involvement of microglia-related molecular networks in the pathophysiology of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
One-hundred nineteen individuals with a family history of AD (Presymptomatic Evaluation of Experimental or Novel Treatments of Alzheimer's Disease [PREVENT-AD] cohort, mean age 67 ± 5 years) underwent tau-PET ([ 18 F]FTP), β-amyloid (Aβ)-PET ([ 18 F]NAV4694 [NAV]), and cognitive assessment. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Poor subjective sleep quality is linked to reduced brain volume and cortical thickness (CTh), but associations with objective sleep measures, particularly regarding sex and AD pathology, remain unclear. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
No amyloid-related imaging abnormalities occurred. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Brain structure in later life reflects both influences of intrinsic aging and those of lifestyle, environment and disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A growing body of literature has suggested that obstructive sleep apnea (OSA) and habitual short sleep duration are linked to poor cognitive function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Among 5757 participants (21.7% Black, 20.3% Latinx, 58.1% AORE), we found lower odds of amyloid positivity in Black (odds ratio [OR]: 0.72, 95% confidence interval [CI]: 0.62-0.83) and Latinx (OR: 0.78, 95% CI: 0.67-0.91) compared to AORE. 4 key findings →
Participants: 5,757 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217-based biomarkers showed excellent detecting performance for early amyloid (Thal I-II; area under the curve values > 0.96) and intermediate tau (Braak III-IV; area under the curve values > 0.92). 5 key findings →
Participants: 237 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of the 944 clinical cases, 13.0% were characterized as probable LATE (2.4% pure LATE and 10.6% LATE+AD) and 23.7% were characterized as probable AD without LATE. 5 key findings →
Participants: 944 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF Aβ42/Aβ40 contributed most to identify Aβ-positivity, while continuous Aβ-PET load within the positive range was best predicted by plasma P-tau217. 1 key finding →
Participants: 1,053 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
EXT showed high cross-sectional reliability and longitudinal stability. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The advent of amyloid-β (Aβ) and tau PET imaging has revolutionized Alzheimer disease (AD) research, enabling in vivo detection of hallmark pathologies and transforming both diagnosis and therapeutic development. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This paper introduces a novel convolutional neural network model with an attention mechanism to advance Alzheimer disease (AD) classification using Magnetic Resonance Imaging (MRI). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
< 0.001), with the automated approach more likely to classify a scan as tau negative and lower agreement between methods in more severe cases and AD clinical variants. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Traditional diagnostic methods for Alzheimer's disease often suffer from low accuracy and lengthy processing times, delaying crucial interventions and patient care. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.120). These findings suggest that DESH and high EI, often considered biomarkers for iNPH, may lack specificity and may be found in a subset of patients with PSP or LBD leading to unnecessary neurosurgery for iNPH. 1 key finding →
Participants: 190 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
< 0.035), consistent with a neurodegenerative pattern. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
16% of individuals were identified as tau-accumulators. 5 key findings →
Design: longitudinal study Participants: 29 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 2,885 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →