ArticleBrain structure & function2026
Neural substrates of cognitive decline and tremor in neuronal intranuclear inclusion disease: a morphometric MRI study.
Article in Brain structure & function, 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
5 authors.
Funding
Abstract
Neuronal intranuclear inclusion disease (NIID) is a rare neurodegenerative disorder characterized primarily by progressive cognitive decline and tremor. While these clinical features are well-recognized, the specific structural neural substrates and morphometric alterations underlying these symptoms remain poorly understood. This prospective study included 10 genetically confirmed NIID patients and 10 age- and sex-matched controls. Following high-resolution T1-weighted MRI and MoCA-based cognitive assessment, atlas-based morphometry was utilized to characterize gray-matter alterations. The analytical workflow prioritized identifying global atrophy patterns between groups, followed by correlation analyses between identified atrophic regions and clinical markers (MoCA scores and disease onset). Additionally, subgroup comparisons were conducted within the patient cohort to identify the neural correlates of tremor. Compared with healthy controls, NIID patients exhibited widespread gray-matter atrophy primarily involving the extensive temporal and occipital cortices, limbic and paralimbic regions (including the cingulate gyri, hippocampus, and amygdala), and the thalamus (Bonferroni-corrected, p < 0.05). Notably, lower MoCA scores were significantly associated with reduced volumes in the left hippocampus and the left temporal pole (extending to the superior and middle temporal gyri) (all p < 0.05). Earlier disease onset was correlated with the relative preservation of the left thalamus (r = -0.755, p = 0.019). Finally, patients manifesting tremor displayed significantly diminished gray-matter volume in the right hippocampus compared to tremor-free patients (t = 2.472, p = 0.039). Distinct morphometric substrates underpin cognitive dysfunction and tremor in NIID. Cognitive decline is primarily associated with atrophy in the left hippocampus and temporal regions, whereas tremor manifestation is linked to right hippocampal volume loss. These findings elucidate the neuroanatomical basis of NIID's core symptoms and highlight regional brain atrophy as a potential imaging biomarker for disease monitoring and future therapeutic trials.
Indexed as
Identifiers
42467106What OpenQuestion 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 OpenQuestion graph.