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Background: The status of the hypothalamic‐pituitary‐gonadal (HPG) axis is important for assessing the onset of physiological or pathological puberty. The reference standard gonadotropin‐releasing hormone (GnRH) stimulation test requires hospital admission and repeated blood samples. A simple noninvasive method would be beneficial. Objectives: To explore a noninvasive method for evaluating HPG axis activation in children using an MRI radiomics model. Study Type: Retrospective. Population: Two hundred thirty‐nine children (83 male; 3.6–14.6 years) with hypophysial MRI and GnRH stimulation tests, randomly divided a training set (168 children) and a test set (71 children). Field Strength/Sequence: 3.0 T, 3D isotropic fast spin echo (CUBE) T1‐weighted imaging (T1WI) sequences. Assessment: Radiomics features were extracted from sagittal 3D CUBE T1WI, and imaging signatures were generated using the least absolute shrinkage and selection operator (LASSO) with 10‐fold cross‐validation. Diagnostic performance for differential diagnosis of HPG status was compared between a radiomics model and MRI features (adenohypophyseal height [aPH] and volume [aPV]). Statistical Tests: Receiver operating characteristic (ROC) and decision curve analysis (DCA). A P value <0.05 was considered statistically significant. Results: Eight hundred fifty‐one radiomics features were extracted and reduced to 10 by the LASSO method in the training cohort. The radiomics model based on CUBE T1WI showed good performance in assessment of HPG axis activation with an area under the ROC curve (AUC) of 0.81 (95% CI: 0.71, 0.91) in the test set. The AUC of the radiomics model was significantly higher than that of aPH (0.81 vs. 0.65) but there was no significant difference compared to aPV (0.81 vs. 0.78, P = 0.58). In DCA analysis, the radiomics signature showed higher net benefit over the aPV and aPH models. Data Conclusions: The MRI radiomics model has potential to assess HPG axis activation status noninvasively, potentially providing valuable information in the diagnosis of patients with pathological puberty onset. Evidence Level: 4 Technical Efficacy: Stage 2 [ABSTRACT FROM AUTHOR]

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Background: Gliomas are highly invasive brain tumors that evade accurate geographic assessment by conventional MRI due to microscopic invasion along white matter (WM) tracts. Advanced diffusion MRI techniques are needed to assess occult WM involvement., Purpose: To evaluate peak width of skeletonized mean diffusivity (PSMD) and peak width of skeletonized free water (PSFW), and axonal water fraction (AWF) for assessing glioma-induced alterations in normal-appearing WM and their relationship with isocitrate dehydrogenase 1 (IDH1) mutation., Study Type: Retrospective., Population: One hundred five glioma patients (46 ± 13 years), 53 healthy controls (HCs) (46 ± 9 years)., Field Strength/sequence: 3.0 T, T1WI, T1-CE, T2WI, T2FLAIR, and DKI., Assessment: PSMD and PSFW were compared between lesion and contralateral sides in glioma patients and between patients and HCs. The associations between these metrics and clinical variables, including IDH1 mutation, was assessed. Corpus callosum (CC) injury, quantified by the AWF, was evaluated for its mediated effect of IDH1 mutation on contralesional PSMD and PSFW., Statistical Tests: Paired-t tests, ANCOVA, univariate and multivariate linear regression, and mediation analysis with significance set at P < 0.05., Results: Contralateral PSMD and PSFW were significantly higher in left-sided gliomas (PSMD: 0.206 ± 0.027 vs. 0.193 ± 0.023; PSFW: 0.119 ± 0.019 vs. 0.106 ± 0.020) than in HCs, with similar increases in right-sided gliomas (PSMD: 0.219 ± 0.036 vs. 0.195 ± 0.023; PSFW: 0.129 ± 0.031 vs. 0.109 ± 0.020). IDH1 wild-type gliomas were associated with higher contralateral PSMD and PSFW (β = -0.302 and -0.412). AWF of CC mediated the impact of IDH1 mutations on contralesional PSMD and PSFW (mediated proportion: 42.7% and 53.7%)., Data Conclusion: PSMD and PSFW are effective biomarkers for assessing WM integrity in gliomas, significantly associated with IDH1 mutation status. AWF of CC mediates the relationship between IDH1 mutation and contralesional PSMD and PSFW., Evidence Level: 4 TECHNICAL EFFICACY: Stage 2., (© 2024 International Society for Magnetic Resonance in Medicine.)

Rationale and Objectives: To investigate iron and myelin changes in deep gray matter (DGM) of relapsing-remitting multiple sclerosis (RRMS) patients and their relationship to atrophy by χ-separation imaging., Materials and Methods: 33 RRMS patients and 34 healthy controls (HC) were included in this study. The χ-separation map reconstructed from a 3D multi-echo gradient echo scan was used to measure the positive susceptibility (χ pos ) and negative susceptibility (χ neg ) of DGM. To take into account the effect of atrophy, susceptibility mass of DGM was calculated by multiplying volume by the mean bulk susceptibility. Differences in MRI metrics between baseline patients, follow-up patients, and HC were compared respectively., Results: Compared to HC, χ pos of basal ganglia were significantly increased in follow-up patients (P < 0.05). The χ pos of pallidum was significantly higher in follow-up patients than that in baseline patients (P = 0.006). The χ neg of caudate, pallidum and hippocampus in baseline and follow-up patients was significantly higher than that in HC (P < 0.05). When taking into account the effect of atrophy, there was a significant decrease in χ pos mass and a significant increase in χ neg mass of thalamus, accumbens and amygdala in follow-up patients compared to HC (P < 0.05). The χ pos mass of the thalamus was further decreased in follow-up patients compared to baseline patients (P = 0.006)., Conclusion: χ-separation imaging could generate independent information on iron and myelin changes in RRMS patients, showing atrophy-dependent iron increase in basal ganglia and atrophy-independent iron and myelin decrease in thalamus., Competing Interests: Declaration of Competing Interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Wenzhen Zhu reports financial support was provided by National Natural Science Foundation of China. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Association of University Radiologists. Published by Elsevier Inc. All rights reserved.)

Abstract: Spinal and bulbar muscular atrophy (SBMA) is a neurodegenerative disease caused by extended CAG trinucleotide repeats in the androgen receptor (AR) gene, which encodes a ligand-dependent transcription factor. The mutant AR protein, characterized by polyglutamine expansion, is prone to misfolding and forms aggregates in both the nucleus and cytoplasm in the brain in SBMA patients. These aggregates alter protein-protein interactions and compromise transcriptional activity. In this study, we reported that in both cultured N2a cells and mouse brain, mutant AR with polyglutamine expansion causes reduced expression of mesencephalic astrocyte-derived neurotrophic factor (MANF). Overexpression of MANF ameliorated the neurotoxicity of mutant AR through the inhibition of mutant AR aggregation. Conversely, knocking down endogenous MANF in the mouse brain exacerbated neuronal damage and mutant AR aggregation. Our findings suggest that inhibition of MANF expression by mutant AR is a potential mechanism underlying neurodegeneration in SBMA., (Copyright © 2025 Copyright: © 2025 Neural Regeneration Research.)

Huntington's disease (HD) is an autosomal dominant neurodegenerative disease characterized by preferential neuronal loss in the striatum. The mechanism underlying striatal selective neurodegeneration remains unclear, making it difficult to develop effective treatments for HD. In the brains of nonhuman primates, we examined the expression of Huntingtin ( HTT ), the gene responsible for HD. We found that HTT protein is highly expressed in striatal neurons due to its slow degradation in the striatum. We also identified tripartite motif-containing 37 (TRIM37) as a primate-specific protein that interacts with HTT and is selectively reduced in the primate striatum. TRIM37 promotes the ubiquitination and degradation of mutant HTT (mHTT) in vitro and modulates mHTT aggregation in mouse and monkey brains. Our findings suggest that nonhuman primates are crucial for understanding the mechanisms of human diseases such as HD and support TRIM37 as a potential therapeutic target for treating HD.