ArticleAlzheimer's research & therapy2026
Characterizing the MRI signature of hippocampal sclerosis of aging.
Article in Alzheimer's research & therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
30 authors.
Funding
Abstract
backgroundHippocampal sclerosis of aging (HS-A), a common cause of dementia, can currently only be diagnosed at autopsy. We aimed to identify and evaluate MRI metrics to distinguish HS-A from Alzheimer's Disease neuropathologic change (ADNC) and cases with limited/no pathology.
methodsHS-A (N = 5), ADNC (N = 10), and limited/no pathology (N = 12) cases were compared on postmortem MRI signatures: manually measured cornu ammonis (CA)1/subiculum thickness, grey matter signal intensity, and automated hippocampal subfield thickness metrics. Similar metrics were obtained in T
resultsPostmortem MRI showed hippocampal thinning and grey matter hypointensity in HS-A at the CA1-subiculum junction more severe than in ADNC and limited/no pathology cases. In antemortem MRI, differentiating HS-A and ADNC based on anterior/posterior manual measures of CA1/subiculum thickness and hippocampal volumes displayed good discrimination in dataset 1, but lower discriminative performance in dataset 2. In complementary analyses pooling both datasets and adjusting for age, manual thickness achieved good performance (area under the curve (AUC) = 0.80-0.87), while anterior, posterior, and whole hippocampal volumes showed excellent discrimination (AUC = 0.94-0.98). LIMITATIONS: The study included a relatively small and neuropathologically heterogeneous sample. The final antemortem analyses were exploratory, reflecting challenges in replicating findings across independent datasets. Classification was limited to HS-A and ADNC, leaving it uncertain how the metrics perform when comparing HS-A with other diagnostic groups. HS-A diagnoses were determined postmortem, often several years after MRI, and most measures relied on standard imaging sequences with limited resolution to assess fine-grained hippocampal subfields.
conclusionsHS-A displays distinct changes in the hippocampus that are detectable through structural MRI. Associated quantifiable MRI metrics may serve as promising tools in aiding antemortem HS-A diagnosis but require further validation in larger cohorts and against other dementia-related diseases.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.