Brain communications最新文献

{"title":"An open-label Phase 2a study to assess the safety and tolerability of trimetazidine in patients with amyotrophic lateral sclerosis.","authors":"Ruben P A van Eijk, Frederik J Steyn, Mark R Janse van Mantgem, Angela Schmidt, Myrte Meyjes, Sally Allen, Dara V Daygon, Jean-Philippe Loeffler, Ammar Al-Chalabi, Leonard H van den Berg, Robert D Henderson, Shyuan T Ngo","doi":"10.1093/braincomms/fcaf063","DOIUrl":"10.1093/braincomms/fcaf063","url":null,"abstract":"<p><p>Metabolic imbalance is associated with amyotrophic lateral sclerosis progression. Impaired glucose oxidation and increased reliance on fatty acid oxidation contribute to reduced metabolic flexibility and faster disease progression in amyotrophic lateral sclerosis. We sought to evaluate the safety and tolerability, and explore the pharmacodynamic response of trimetazidine, a partial fatty acid oxidation inhibitor, on oxidative stress markers and energy expenditure in amyotrophic lateral sclerosis. The study was conducted between June 29, 2021 and May 24, 2023. People living with amyotrophic lateral sclerosis, recruited in Australia and the Netherlands, received open-label oral trimetazidine for 12 weeks after an initial 4-week lead-in period. The primary outcome measures were safety and tolerability, as well as the change from baseline in oxidative stress markers malondialdehyde (MDA) and 8-hydroxy-2'-deoxyguanosine (8-OHdG). Secondary outcome measures were change from baseline in energy expenditure, amyotrophic lateral sclerosis functional rating scale-revised, and slow vital capacity (SVC). Linear mixed effects were used to estimate the mean difference in MDA and 8-OHdG between the on- and off-treatment periods. This trial is registered under ClinicalTrial.gov National Clinical Trial (NCT) number NCT04788745 and European Union Drug Regulating Authorities Clinical Trials (EudraCT) number 2020-005018-17. Twenty-one participants received trimetazidine; 19 (90%) completed the treatment period. Trimetazidine was well tolerated; there were 57 adverse events reported, of which 7 (11%) were deemed potentially drug-related, including hot flushes (2), nausea (2), paraesthesia (2) and fatigue (1). MDA was numerically lower during treatment [-0.29 uM; 95% confidence interval (CI) -0.90 to 0.33, <i>P</i>  <i>=</i> 0.36]; 8-OHdG was significantly lower during treatment (-0.12 nM; 95% CI -0.23 to -0.01, <i>P</i> = 0.0245). The decrease in oxidative stress markers was accompanied by a reduction in resting energy expenditure (95 kcal, 95% CI 36.8-154, <i>P</i> = 0.0014). The absence of a placebo group prevented the interpretation of the clinical parameters. Oral trimetazidine was safe and well tolerated among patients with amyotrophic lateral sclerosis. This, combined with the significant reduction in markers of oxidative stress and resting energy expenditure, warrants a larger double-blind placebo-controlled efficacy study.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf063"},"PeriodicalIF":4.1,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11851067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143506056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Navigating neural pathways: how stimulation polarity shapes deep brain stimulation efficacy.","authors":"Atefeh Asadi, Nabin Koirala, Muthuraman Muthuraman","doi":"10.1093/braincomms/fcaf061","DOIUrl":"10.1093/braincomms/fcaf061","url":null,"abstract":"<p><p>This scientific commentary refers to 'Neural pathway activation in the subthalamic region depends on stimulation polarity' by Borgheai <i>et al</i>. (https://doi.org/10.1093/braincomms/fcaf006).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf061"},"PeriodicalIF":4.1,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11839837/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143470293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulating nociception networks: the impact of low-intensity focused ultrasound on thalamocortical connectivity.","authors":"Arabinda Mishra, Pai-Feng Yang, Thomas J Manuel, Allen T Newton, M Anthony Phipps, Huiwen Luo, Michelle K Sigona, Allison Q Dockum, Jamie L Reed, John C Gore, William A Grissom, Charles F Caskey, Li Min Chen","doi":"10.1093/braincomms/fcaf062","DOIUrl":"10.1093/braincomms/fcaf062","url":null,"abstract":"<p><p>Pain engages multiple brain networks, with the thalamus serving as a critical subcortical hub. This study aims to explore the effects of low-intensity transcranial focused ultrasound-induced suppression on the organization of thalamocortical nociceptive networks. We employed MR-guided focused ultrasound, a potential non-invasive therapy, with real-time ultrasound beam localization feedback and fMRI monitoring. We first functionally identified the focused ultrasound target at the thalamic ventroposterior lateral nucleus by mapping the whole-brain blood oxygenation level-dependent responses to nociceptive heat stimulation of the hand using fMRI in each individual macaque monkey under light anaesthesia. The blood oxygenation level-dependent fMRI signals from the heat-responsive thalamic ventroposterior lateral nucleus were analysed to derive thalamocortical effective functional connectivity network using the psychophysical interaction method. Nineteen cortical regions across sensorimotor, cognitive, associative and limbic networks exhibited strong effective functional connectivity to the thalamic ventroposterior lateral during heat nociceptive processing. Focused ultrasound-induced suppression of heat activity in the thalamic ventroposterior lateral nucleus altered nociceptive responses in most of the 19 regions. Data-driven hierarchical clustering analyses of blood oxygenation level-dependent time courses across all thalamocortical region-of-interest pairs identified two effective functional connectivity subnetworks. The concurrent suppression of thalamic heat response with focused ultrasound reorganized these subnetworks and modified thalamocortical connection strength. Our findings suggest that the thalamic ventroposterior lateral nucleus has extensive and causal connections to a wide array of cortical areas during nociceptive processing. The combination of MR-guided focused ultrasound with fMRI enables precise dissection and modulation of nociceptive networks in the brain, a capability that no other device-based neuromodulation methods have achieved. This presents a promising non-invasive tool for modulating pain networks with profound clinical relevance. The robust modulation of nociceptive effective functional connectivity networks by focused ultrasound strongly supports the thalamic ventroposterior lateral as a viable target for pain management strategies.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf062"},"PeriodicalIF":4.1,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878384/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Brain aging rejuvenation factors in adults with genetic and sporadic neurodegenerative disease.","authors":"","doi":"10.1093/braincomms/fcaf058","DOIUrl":"https://doi.org/10.1093/braincomms/fcaf058","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.1093/braincomms/fcae432.].</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf058"},"PeriodicalIF":4.1,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11803422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143384481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The inflammatory APRIL (a proliferation-inducing ligand) antagonizes chondroitin sulphate proteoglycans to promote axonal growth and myelination.","authors":"Mashal Claude Ahmed, Tejaswini Kakunuri, Leticia Peris, Delphine Meffre, Elif Nur Yilmaz, Laureen Grewing, Raquel Guerrero González, Benoit Manfroi, Evelyne Gout, Romain R Vivès, Una Fitzgerald, Pascal Schneider, Mehrnaz Jafarian-Tehrani, Tanja Kuhlmann, Bertrand Huard","doi":"10.1093/braincomms/fcae473","DOIUrl":"10.1093/braincomms/fcae473","url":null,"abstract":"<p><p>Lesions in the CNS are frequently associated to a detrimental inflammatory reaction. In autoimmune neurodegenerative diseases, a proliferation-inducing ligand (APRIL) produced by CNS-infiltrating inflammatory cells binds to chondroitin sulphate proteoglycans (CSPGs). The latter are well-established obstacles to neural regeneration and remyelination in the CNS by interacting with receptor protein tyrosine phosphatase (RPTP) and Nogo receptor (NgR) families. Here, we are showing that APRIL blocks the interactions of RPTP and NgR with all types of chondroitin sulphate (CS). Functionally, APRIL neutralized the inhibitory effects of CS on mouse and human neuronal process growth. APRIL also blocked the inhibition of CS on mouse and human oligodendrocyte differentiation. Finally, APRIL increased myelination in an <i>ex vivo</i> organotypic model of demyelination in the presence of endogenous CSPG upregulation. Our data demonstrate the potential value for a recombinant form of soluble APRIL to achieve repair in the CNS.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcae473"},"PeriodicalIF":4.1,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11803424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding Alzheimer's disease: acetylcholine and dopamine pathway disruptions as early markers of cognitive decline.","authors":"Claudio Zaccone, Annalisa Nobili, Marcello D'Amelio","doi":"10.1093/braincomms/fcaf057","DOIUrl":"10.1093/braincomms/fcaf057","url":null,"abstract":"<p><p>This scientific commentary refers to 'Changes in neurotransmitter-related functional connectivity along the Alzheimer's disease continuum', by Manca <i>et al</i>. (https://doi.org/10.1093/braincomms/fcaf008).</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf057"},"PeriodicalIF":4.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11840162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143470263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"<i>HTT, ATXN1</i> and <i>ATXN2</i> CAG triplet repeat sizes: exploring their role in the disease risk and cancer comorbidity in Parkinson's disease.","authors":"Sergio Pérez-Oliveira, Ignacio Álvarez, Manuel Menéndez-González, Israel David Duarte-Herrera, Marta Blázquez-Estrada, Juan Castilla-Silgado, Esther Suárez, Ciara García-Fernández, Pablo Siso-García, Pablo García-González, Maitee Rosende-Roca, Mercè Boada, Agustín Ruiz, Jon Infante, Beatriz De la Casa-Fages, Isabel González-Aramburu, Victoria Álvarez, Pau Pastor","doi":"10.1093/braincomms/fcaf060","DOIUrl":"10.1093/braincomms/fcaf060","url":null,"abstract":"<p><p>Parkinson's disease genetic embraces genetic and non-genetic factors. It has been suggested a link between CAG repeat number in the <i>HTT, ATXN1</i> and <i>ATXN2</i> genes and different neurodegenerative diseases. Several genetic factors involved in Parkinson's disease development are indeed associated with cancer pathways. Moreover, several studies found a low prevalence of cancer in neurodegenerative diseases that can be associated with a low CAG repeat size in several genes. This study aimed to investigate the influence of CAG repeat sizes in <i>ATXN1, ATXN2</i> and <i>HTT</i> genes on the risk for developing cancer and Parkinson's disease in a large cohort of patients with idiopathic Parkinson's disease and healthy controls. The work included 1052 patients with idiopathic Parkinson's disease and 1070 controls of European ancestry. CAG repeat sizes in <i>HTT, ATXN1</i> and <i>ATXN</i>2 genes were analysed. Dunn's multiple comparison test for quantitative variables and logistic and linear regression were used. The long <i>ATXN1</i> and <i>HTT</i> alleles and CAG size and both the <i>ATXN2</i> short and long alleles were predictors for the Parkinson's disease risk. The long CAG <i>ATXN1</i> allele gene was associated with the risk of cancer. No association was observed between CAG size in the <i>HTT</i> and <i>ATXN2</i> genes and risk of cancer in patients with Parkinson's disease. We described an association of <i>HTT, ATXN1</i> and <i>ATXN2</i> with the risk of Parkinson's disease, which reinforce the hypothesis of the common pathway of neurodegeneration. Besides, <i>ATXN1</i> could be a predictor of cancer risk among patients with Parkinson's disease, and these results suggest that cancer and neurodegeneration processes can share common pathways.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf060"},"PeriodicalIF":4.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11837329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143461086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brainstem and cerebellar radiological findings in progressive supranuclear palsy.","authors":"Chloe Spiegel, Cassandra Marotta, Kelly Bertram, Lucy Vivash, Ian H Harding","doi":"10.1093/braincomms/fcaf051","DOIUrl":"10.1093/braincomms/fcaf051","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Progressive supranuclear palsy is a sporadic neurodegenerative 4-repeat tauopathy associated with significant morbidity. Heterogeneity of symptom expression among this group is increasingly recognized, reflecting variable tau spread and neurodegeneration. Clinical manifestations consist of debilitating and rapidly progressive motor, oculomotor, speech, cognitive and affective impairments. Core pathological changes are noted with a predominance in the midbrain and basal ganglia; however, spread to the more caudal brainstem and cerebellar regions is reported at various stages. Accordingly, whilst midbrain atrophy is the best recognized supportive imaging finding, quantitative neuroimaging studies using MRI and PET approaches have revealed a wider profile of brain abnormalities in cohorts of individuals with progressive supranuclear palsy. This expanded neurobiological scope of disease may account for individual heterogeneity and may highlight additional biological markers that are relevant to diagnosing and tracking the illness. Additionally, there is increasing understanding of the diverse cognitive, affective and speech functions of the cerebellum, which may be implicated in progressive supranuclear palsy beyond current recognition. In this review, we undertake a systematic literature search and summary of &lt;i&gt;in vivo&lt;/i&gt; structural and functional neuroimaging findings in the brainstem and cerebellum in progressive supranuclear palsy to date. Novel and multimodal imaging techniques have emerged over recent years, which reveal several infratentorial alterations beyond midbrain atrophy in progressive supranuclear palsy. Most saliently, there is evidence for volume loss and microstructural damage in the pons, middle cerebellar peduncles and cerebellar cortex and deep nuclei, reported alongside recognized midbrain and superior cerebellar peduncle changes. Whilst the literature supporting the presence of these features is not unanimous, the evidence base is compelling, including correlations with disease progression, severity or variant differences. A smaller number of studies report on abnormalities in MRI measures of iron deposition, neuromelanin, viscoelasticity and the glymphatic system involving the infratentorial regions. Molecular imaging studies have also shown increased uptake of tau tracer in the midbrain and cerebellar dentate nucleus, although concern remains regarding possible off-target binding. Imaging of other molecular targets has been sparse, but reports of neurotransmitter, inflammatory and synaptic density alterations in cerebellar and brainstem regions are available. Taken together, there is an established evidence base of &lt;i&gt;in vivo&lt;/i&gt; imaging alterations in the brainstem and cerebellum which highlights that midbrain atrophy is often accompanied by other infratentorial alterations in people with progressive supranuclear palsy. Further research examining the contribution of these features to clinical morbidity and inter-indi","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf051"},"PeriodicalIF":4.1,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating genome-wide association studies and transcriptomics prioritizes drug targets for meningioma.","authors":"Wan-Zhe Liao, Jia-He Wang, Hua-Jie Zhong, Shen-Yu Wen, Yang Chen, Jia-Qi Chen, Xue-Kun Zhang, Xin-Yi Wu, Jia-Nuo Tan, Kun-Yi Li, Shao-Cong Mo, Li-Jun Wang","doi":"10.1093/braincomms/fcaf053","DOIUrl":"10.1093/braincomms/fcaf053","url":null,"abstract":"<p><p>Meningioma, a prevalent central nervous system tumour, presents a significant challenge in neuro-oncology. This study harnesses genome-wide association studies (GWAS) and transcriptomic analysis to illuminate the pathological underpinnings of meningioma and spearhead the discovery of novel drug targets. By employing summary-data-based Mendelian randomization (SMR), colocalization analyses and Mendelian randomization, we pinpointed four genes as pivotal therapeutic targets. The integration of bulk and single-cell RNA sequencing confirmed the upregulated expression of three of the genes (<i>XBP1</i>, <i>TTC28</i> and <i>TRPC6</i>) in meningioma tissues, unravelling their cellular distribution and hinting at the tumour's intrinsic heterogeneity. Molecular docking further identified dexamethasone and levonorgestrel as potential modulators of these targets, paving the way for personalized meningioma treatment strategies. This research advances our understanding of meningioma's molecular landscape and illustrates the power of genomic and transcriptomic integration in the realm of precision oncology.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 2","pages":"fcaf053"},"PeriodicalIF":4.1,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11880806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143568985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of dehydroepiandrosterone sulphate levels on the slower age-related decline in grey matter in younger women with polycystic ovary syndrome.","authors":"Mei-Jou Chen, Chang-Le Chen, Yu-Yuan Chang, Chu-Chun Huang, Wen-Chau Wu, Hong-Nerng Ho, Wen-Yih Isaac Tseng","doi":"10.1093/braincomms/fcaf052","DOIUrl":"10.1093/braincomms/fcaf052","url":null,"abstract":"<p><p>Polycystic ovary syndrome (PCOS) is characterized by excess androgens, ovulatory disorders and a higher prevalence of obesity and metabolic disturbances including Type 2 diabetes, hyperlipidaemia and hypertension, some of which are risk factors for neurodegenerative disorders such as Alzheimer's disease and brain atrophy. However, it is unclear whether brain ageing occurs more rapidly in women with PCOS compared with those without PCOS. Except for the hypothalamic-pituitary-gonadal axis involved in the conventional ovulatory process, little is known regarding the role of the grey matter in the pathogenesis of PCOS, and limited existing studies examining brain structures in PCOS have shown inconsistent results. This case-control study aimed to investigate the age-related differences in total and regional brain grey matter volume and average cortical thickness in young women with and without PCOS by using brain magnetic resonance imaging to understand whether women with PCOS exhibit distinctive patterns of brain ageing, and their association with factors including obesity, hyperandrogenism and metabolic disturbances. Seventy-six women diagnosed with PCOS and 68 age-matched women without PCOS (aged 20-35 years) underwent brain magnetic resonance imaging to measure grey matter volume and cortical thickness. Anthropometric, hormonal and metabolic measurements were conducted to assess their associations with the investigated brain structures. In women without PCOS, increasing age was significantly correlated with a decrease in global grey matter volume (<i>r</i> = -0.5598, <i>P</i> < 0.0001), while this association was not significant in women with PCOS (<i>r</i> = -0.1475, <i>P</i> = 0.204). The decline in grey matter volume with age differed significantly between the two groups regardless of obesity (body mass index exceeding 25 kg/m²), especially in the frontal, parietal, occipital and temporal regions. After adjusting for dehydroepiandrosterone sulphate (DHEAS) levels, the negative association between age and global grey matter volume became statistically significant in women with PCOS. Increasing age was also significantly associated with a decrease in global cortical thickness in women without PCOS, but not in women with PCOS. Such negative association between global cortical thickness and age was particularly stronger in women with obesity compared with those without. The negative association between age and global cortical thickness in women with PCOS became pronounced after adjusting for DHEAS levels. Women with PCOS experience a milder grey matter loss with age compared with women without PCOS. The neuroprotective effect of high DHEAS levels in women with PCOS may be implicated in this relationship.</p>","PeriodicalId":93915,"journal":{"name":"Brain communications","volume":"7 1","pages":"fcaf052"},"PeriodicalIF":4.1,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11829216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143434695","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}