Brain disorders (Amsterdam, Netherlands)最新文献

{"title":"Pattern of central nervous system related diseases and deaths: a 10-year study in a Ghanaian tertiary care facility","authors":"Ansumana Bockarie ,&nbsp;Richael Odarkor Mills ,&nbsp;Kofi Ulzen-Appiah ,&nbsp;Albert Akpalu ,&nbsp;Cecelia Smith-Togobo ,&nbsp;Bernice Akua Frimpong ,&nbsp;Ishmael Obeng-Ofosu ,&nbsp;George Nkrumah Osei ,&nbsp;Josephine Anterkyi Bentil ,&nbsp;Patrick Adu ,&nbsp;David Larbi Simpong","doi":"10.1016/j.dscb.2025.100300","DOIUrl":"10.1016/j.dscb.2025.100300","url":null,"abstract":"<div><h3>Background</h3><div>Neurological disorders can have a significant impact on mortality rates. Despite the prevalence of central nervous system related diseases (CNSDs) in Ghana, limited information exists regarding their contribution to death. This study sought to characterize death patterns of patients with CNSDs in a Ghanaian tertiary hospital.</div></div><div><h3>Methods</h3><div>A cross-sectional study was conducted utilizing archival mortality data from 2010 to 2019, retrieved from the mortuary logbook of the Cape Coast Teaching Hospital. Variables such as age, sex, and cause of death were expressed as proportions. Line graphs were used to visualize temporal trends in death cases, while bar graphs were used to illustrate the distribution of various conditions constituting CNSDs. Binary logistic regression was applied to identify associations between demographic factors and cerebrovascular accident (CVA) associated deaths.</div></div><div><h3>Results</h3><div>A total of 9356 deaths were recorded between 2010 and 2019 of which CNSDs contributed 454 (4.9 %). The majority of deaths resulting from CNSDs were contributed by cerebrovascular accidents (CVAs) 93 % (424/454). Within the study area, more females (51.4 %) died from CVAs than males (49.6 %). Logistic regression analysis further revealed that individuals aged above 60 years had the highest odds of dying from CVAs (OR 48.2, CI 10.9–212.7, <em>p</em> &lt; 0.001) followed by persons aged 40–60 years (OR = 40.4, CI 8.1–200.7, <em>p</em> &lt; 0.001) compared to those below 40 years old.</div></div><div><h3>Conclusion</h3><div>Cerebrovascular accident was the leading cause of death resulting from CNSDs in this study, particularly among individuals aged 40 and above. To address this burden, regular screenings and public education is recommended.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100300"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145571905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Heterozygous FBXO7 as potential genetic modifiers in early-onset Parkinson’s disease with levodopa responsive non-motor features","authors":"Lorenzo Malfer ,&nbsp;Andrea Giorgi ,&nbsp;Tina Liu ,&nbsp;Capucine Piat ,&nbsp;Ali Zare Dehnavi ,&nbsp;Owen A. Ross ,&nbsp;Zhiyv Niu ,&nbsp;Eduardo E. Benarroch ,&nbsp;James H. Bower ,&nbsp;Rodolfo Savica","doi":"10.1016/j.dscb.2025.100305","DOIUrl":"10.1016/j.dscb.2025.100305","url":null,"abstract":"<div><h3>Objective</h3><div>To report a retrospective clinical series of four patients diagnosed with early-onset Parkinson’s disease (EOPD) carrying heterozygous variants of uncertain significance (VUSs) in the <em>FBXO</em>7 gene.</div></div><div><h3>Background</h3><div><em>FBXO</em>7 encodes an F-box-domain-containing protein involved in the mitophagy process, and mutations in this gene have been associated with PARK15, an atypical form of Parkinson’s disease (PD) with an autosomal recessive inheritance pattern.</div></div><div><h3>Methods</h3><div>Patients were identified using the <em>Mayo Clinic Data Explorer</em>. All the cases with a heterozygous <em>FBXO</em>7 variant and a clinical diagnosis of EOPD evaluated at Mayo Clinic between 2017 and 2024 were included. Clinical features, genetic testing, imaging, and treatment data were obtained retrospectively from medical records review. Motor symptoms were assessed using the UPDRS part-III score, and non-motor symptoms were assessed using the NMSS score.</div></div><div><h3>Results</h3><div>Four patients met the inclusion criteria. All exhibited a non-motor predominant phenotype, with significant autonomic features either as an early presentation or as a preeminent component. These features manifested with a broad spectrum of symptoms including sialorrhea, constipation, urinary urgency, orthostatic intolerance and altered heat sensitivity. DaTscan imaging, available in three of the four cases, was consistent with a PD diagnosis. All patients responded well to levodopa treatment, showing substantial improvement in both motor and non-motor symptoms (NMSS).</div></div><div><h3>Conclusion</h3><div><em>FBXO</em>7 may play a role as a phenotypic gene modifier and contribute to the development of EOPD characterized by levodopa-responsive, non-motor-predominant features in heterozygous variant carriers. Specifically, these features appear to be associated with central autonomic dysfunction, particularly affecting the parasympathetic vagal nuclei.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100305"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145977035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between tuberculosis and Guillain–Barré syndrome: a systematic review","authors":"Chowdhury Adnan Sami ,&nbsp;Refaya Tasnim ,&nbsp;Husna Rafsana ,&nbsp;Joydip Chowdhury ,&nbsp;Samiha Jabin Susmita ,&nbsp;Anika Tabassum ,&nbsp;Mohammad Ferdous Ur Rahaman ,&nbsp;Shohael Mahmud Arafat","doi":"10.1016/j.dscb.2025.100299","DOIUrl":"10.1016/j.dscb.2025.100299","url":null,"abstract":"<div><h3>Background</h3><div>Tuberculosis (TB) is highly prevalent in low- and middle-income countries and may present with diverse neurological complications. Its possible association with Guillain–Barré Syndrome (GBS) is rarely reported, but recognition is important because it poses diagnostic challenges and has impotant implications for management in endemic settings.</div></div><div><h3>Methods</h3><div>We systematically reviewed literature from PubMed, Scopus, Google Scholar, Web of Science, and Semantic Scholar (to December 2024) following PRISMA guidelines.</div></div><div><h3>Results</h3><div>We identified 29 cases of TB-associated GBS, with the highest number reported from India (44.8 %). Pulmonary TB was the predominant form (62.1 %), with acute inflammatory demyelinating polyneuropathy (AIDP, 20.7 %) most common. A majority (60.7 %) developed GBS within two weeks of TB symptom onset. Clinical outcomes included complete recovery in 58.6 % and mortality in 17.2 %.</div></div><div><h3>Conclusion</h3><div>Current evidence is limited to case reports and small series, suggesting TB may potentially act as a trigger for GBS, but causality remains unproven. Further controlled studies are needed to clarify mechanisms and outcomes.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100299"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145618461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lidocaine mitigates cognitive decline in elderly patients after video-assisted thoracoscopic surgery: A double-blind randomized controlled clinical trial","authors":"Wang Yong ,&nbsp;Xu Xiaoqiang ,&nbsp;Jing Yibing ,&nbsp;Huang Jian ,&nbsp;Yu Lizhong","doi":"10.1016/j.dscb.2026.100308","DOIUrl":"10.1016/j.dscb.2026.100308","url":null,"abstract":"<div><h3>Background</h3><div><strong>:</strong> Postoperative cognitive decline (POCD) can occur in elderly patients after surgery and is associated with poor outcomes. Lidocaine is an antiarrhythmic and anesthetic agent, with analgesic and anti-inflammatory properties. We aimed to explore the influence of lidocaine on POCD in elderly patients undergoing video-assisted thoracoscopic lobectomy.</div></div><div><h3>Methods</h3><div><strong>:</strong> This was a prospective double-blind randomized controlled clinical trial performed between January 2022 and August 2024. Eligible patients ≥ 65 years old scheduled for video-assisted pulmonary lobectomy under general anesthesia with one-lung ventilation were randomized into lidocaine (1.5 mg/kg lidocaine at anesthesia induction followed by continuous intravenous infusion at 1.5mg/kg/hr) or control (same dose of normal saline) group. Mini-Mental State Examination (MMSE), serum IL-6 and S100β levels, and cerebral oxygen extraction rate (CREO₂) were measured before and after surgery.</div></div><div><h3>Results</h3><div><strong>:</strong> A total of 80 patients, with 40 patients in each group, completed the trial. Compared with pre-operation, MMSE scores in control group were significantly decreased on postoperative days 1 and 3 (<em>P</em> &lt; 0.05), which was mitigated in lidocaine group. Serum IL-6 and S100β levels were significantly increased in control group on postoperative days 1 and 3 (<em>P</em> &lt; 0.05), which was also mitigated in lidocaine group. In addition, CERO₂ was significantly increased in 30 and 60 min after initiation of one-lung ventilation in control group (<em>P</em> &lt; 0.05), which was also mitigated in lidocaine group.</div></div><div><h3>Conclusion</h3><div><strong>:</strong> Lidocaine could mitigate cognitive decline after video-assisted thoracoscopy with one-lung ventilation. Its effect might be related to anti-neuroinflammation and reduced cerebral oxygen metabolic rate.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100308"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146077247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Augmented intelligence in aneurysm care: A systematic review and meta-analysis of diagnostic performance in intracranial aneurysm rupture risk assessment","authors":"Shahin Naghizadeh ,&nbsp;Maryam Zohrabi-Fard ,&nbsp;Mohammad Khorramdin ,&nbsp;Roozbeh Tavanaei ,&nbsp;Kaveh Oraii-Yazdani ,&nbsp;Mona Tamaddon ,&nbsp;Hamed Javadian ,&nbsp;Alireza Zali ,&nbsp;Saeed Oraee-Yazdani","doi":"10.1016/j.dscb.2026.100312","DOIUrl":"10.1016/j.dscb.2026.100312","url":null,"abstract":"<div><h3>Background</h3><div>Accurate assessment of intracranial aneurysm rupture risk remains challenging, with conventional clinical scores showing limited predictive performance. Artificial intelligence (AI) has emerged as a potential adjunct to imaging-based risk stratification, yet the relative performance of AI, human experts, and Human–AI collaboration has not been systematically quantified.</div></div><div><h3>Methods</h3><div>A systematic review and meta-analysis were conducted in accordance with PRISMA guidelines. PubMed, Scopus, Web of Science, and Embase were searched. Studies comparing AI-alone, human-alone, or Human–AI approaches for intracranial aneurysm rupture status or rupture-related risk assessment were included. The outcomes of interest were sensitivity, specificity, accuracy, and the area under the receiver operating characteristic curve (AUC). Random-effects models were applied when appropriate, and methodological quality was assessed using the ROBINS-I tool.</div></div><div><h3>Results</h3><div>Seventeen studies were included. AI-alone models demonstrated consistently high diagnostic performance across sensitivity, accuracy, and AUC, although substantial heterogeneity was observed across methodologies and imaging modalities. Human reader sensitivity varied according to expertise, with expert readers achieving higher sensitivity than non-experts but similar overall accuracy. Human–AI collaborative approaches showed high diagnostic metrics in individual studies; however, the number of eligible studies was limited, and integration strategies were heterogeneous, precluding definitive pooled comparisons.</div></div><div><h3>Conclusions</h3><div>Current evidence indicates that AI models can achieve high diagnostic performance in intracranial aneurysm rupture risk assessment and may serve as a valuable adjunct to clinical expertise. While Human–AI collaboration shows promise, available data remain exploratory and strategy-dependent. Standardized outcome definitions and multicenter prospective studies are required before firm conclusions regarding comparative effectiveness or clinical superiority can be established.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100312"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147421367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic characterisation of ATXN2 in Australian amyotrophic lateral sclerosis","authors":"Sharlynn S.L. Wu ,&nbsp;Emily P. McCann ,&nbsp;Sandrine Chan Moi Fat ,&nbsp;Natalie Grima ,&nbsp;Lyndal Henden ,&nbsp;Liam G. Fearnley ,&nbsp;Patrick Chiu ,&nbsp;Kelly L. Williams ,&nbsp;Dominic B. Rowe ,&nbsp;Garth A. Nicholson ,&nbsp;Matthew C. Kiernan ,&nbsp;Ian P. Blair ,&nbsp;Shu Yang ,&nbsp;Jennifer A. Fifita","doi":"10.1016/j.dscb.2025.100301","DOIUrl":"10.1016/j.dscb.2025.100301","url":null,"abstract":"<div><div>Large expansions of a trinucleotide repeat encoding a polyglutamine tract in <em>ATXN2</em> are a known cause of spinocerebellar ataxia 2, and intermediate length expansions in this gene have been reported as a risk factor and phenotypic modifier for amyotrophic lateral sclerosis (ALS). Here we present a comprehensive analysis of the genetic contribution of <em>ATXN2</em> to ALS within an Australian cohort of 821 ALS cases. We performed association for both disease status and ALS clinical phenotypes, with careful consideration of repeat size and composition, and the presence of additional genetic variants within <em>ATXN2</em>. The largest expansion detected among cases was 33 repeat units, and 32 in controls, while the most common repeat size was 22. Intermediate expansions of 30–33 repeats were significantly more common in ALS cases (1.95 %) than controls (0.42 %, <em>p</em> = 0.02543), and we found this association to be primarily driven by familial rather than sporadic ALS cases (frequency of 4.30 % vs 1.65 % and <em>p</em> = 0.00790 vs 0.05799). All intermediate expansions in ALS cases harboured at least one CAA synonymous interruption. No association was found between intermediate expansions and site or age of disease onset, or disease duration. However, larger intermediate repeat sizes of 32–33 repeats were associated with a shorter disease duration (median=27.35 months) when compared with cases who harboured an <em>ATXN2</em> repeat size in the normal range (median=35.47 months, <em>p</em> = 1.89 × 10^–6). These findings indicate that intermediately expanded <em>ATXN2</em> repeats may play an important gene modifier role in Australian ALS cohorts.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100301"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145618462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Erratum regarding previously published article","authors":"","doi":"10.1016/j.dscb.2026.100307","DOIUrl":"10.1016/j.dscb.2026.100307","url":null,"abstract":"","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100307"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147538440","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CRISPR-Cas9 gene editing in neuropsychiatric disorders: Challenges and promising avenues","authors":"Nicholas Aderinto ,&nbsp;Gbolahan Olatunji ,&nbsp;Emmanuel Kokori ,&nbsp;Ismaila Ajayi Yusuf ,&nbsp;Moradeyo Abdulrahmon ,&nbsp;Emmanuel Egbunu ,&nbsp;Temiloluwa Oluwakorede Adefusi ,&nbsp;Opabode Mountain Obasanjo ,&nbsp;John Aboje ,&nbsp;Ikponmwosa Jude Ogieuhi ,&nbsp;Oluwatobiloba Oluwatomisin Apampa","doi":"10.1016/j.dscb.2025.100304","DOIUrl":"10.1016/j.dscb.2025.100304","url":null,"abstract":"<div><div>This review explores the transformative potential of CRISPR-Cas9 gene editing technology in neuropsychiatric disorders. Neuropsychiatric conditions, marked by genetic and environmental factors, pose significant global health challenges. Traditional treatments often address symptoms, leaving underlying genetic anomalies untouched. CRISPR-Cas9, renowned for its unparalleled precision, presents an opportunity to unravel the complex genetic architecture contributing to disorders like schizophrenia, bipolar disorder, major depressive disorder, autism spectrum disorder (ASD), and attention-deficit/hyperactivity disorder (ADHD). The review explores specific applications of CRISPR technology, showcasing studies targeting genes associated with these disorders and exploring alternative splicing mechanisms, microexon involvement, and the role of master regulators. Despite the revolutionary promise of CRISPR, challenges and limitations must be addressed. Technical challenges, such as achieving allele-specific modifications and minimising off-target effects, require ongoing research. Safety concerns, ethical considerations regarding germline editing, and potential unintended consequences emphasise the need for cautious implementation. Ongoing research aims to refine CRISPR techniques, enhance precision, and overcome current challenges. Collaboration between scientists, ethicists, clinicians, and patient advocacy groups is pivotal for responsible implementation. Identifying specific genes or pathways for therapeutic targeting holds promise for personalised and precise interventions. This review envisions a future where the responsible integration of CRISPR technology transforms the understanding and treatment of neuropsychiatric disorders, providing a multidimensional approach that balances scientific innovation with ethical considerations.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100304"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145737014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of the predictive value of vomiting versus physical examination for a CT scan in children with head injury","authors":"Ali Tarabeih ,&nbsp;Karine Beiruti Wiegler ,&nbsp;Bian Abu Salah ,&nbsp;Doua Bakry","doi":"10.1016/j.dscb.2026.100311","DOIUrl":"10.1016/j.dscb.2026.100311","url":null,"abstract":"<div><h3>Background</h3><div>Head injuries are common in children of all ages. While most are minor and do not require intervention, severe cases remain a leading cause of mortality and disability. Identifying minor head trauma with a significant risk of intracranial injury is challenging. Vomiting is a frequent symptom after pediatric head injury, but its predictive value for intracranial pathology remains uncertain. This study investigates the relationship between vomiting and pathological CT findings in children with head injury.</div></div><div><h3>Methods</h3><div>We conducted a retrospective single-center study of 655 children aged 1-18 with minor head injuries who presented to the pediatric emergency department (2019-2021). Physical examination abnormalities were analyzed as a composite variable. Logistic regression identified predictors of pathological CT findings among children with vomiting.</div></div><div><h3>Results</h3><div>Vomiting occurred in 30.9% of patients. CT rates and pathological findings were similar between children with vomiting (41.1% scanned, 22.9% with pathology) and those without vomiting (38.6% scanned, 21.1% with pathology). Among children with vomiting who underwent CT, composite physical examination abnormalities predicted pathological findings (OR=14.2, 95% CI: 1.75–114.68). However, these variable combined heterogeneous findings from minor scalp hematomas to neurological deficits, limiting interpretation.</div></div><div><h3>Conclusions</h3><div>Vomiting alone was not associated with increased pathological CT findings. Composite physical examination abnormalities predicted CT pathology in children with vomiting. Major limitations include the composite nature of the variable, lack of CT or follow-up in 60.5% of patients, incomplete vomiting data, and selection bias in imaging. Prospective studies with validated criteria and systematic follow-up are needed to confirm observation safety.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100311"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147421368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integration of the serum metabolome and gut microbiome underscores the importance of altered lipid metabolism and potential immune modulation in Parkinson's Disease","authors":"Keren Zhang ,&nbsp;Kimberly C Paul ,&nbsp;Jonathan P Jacobs ,&nbsp;Yuyuan Lin ,&nbsp;Dayoon Kwon ,&nbsp;Roch Nianogo ,&nbsp;Jeff M Bronstein ,&nbsp;Adrienne M Keener ,&nbsp;Yu Yu ,&nbsp;Aline Duarte Folle ,&nbsp;Dean P Jones ,&nbsp;Beate Ritz","doi":"10.1016/j.dscb.2026.100310","DOIUrl":"10.1016/j.dscb.2026.100310","url":null,"abstract":"<div><h3>Introduction</h3><div>Single-omics studies have deepened our understanding of disease-related molecular processes, though integrated approaches are needed to uncover cross-system interactions. We previously reported changes in the serum metabolome and gut microbiome in Parkinson’s disease (PD). To build on these findings, we conducted a multi-omics integration analysis to examine the interplay between the gut microbiome and human metabolism in PD.</div></div><div><h3>Methods</h3><div>In a community-based study of 113 PD patients from rural California, microbiome profiles were obtained via 16S rRNA gene sequencing of fecal samples. Serum metabolomic profiles were generated using untargeted high-resolution LC-MS. Residual matrices of metabolomics data were extracted after adjusting for age, sex, racial minority status, and study wave. We identified PD-associated bacterial genera and summarized their abundance using principal component analysis. Using this summary score as the dependent variable, we performed partial least squares (PLS) regression to identify serum metabolites associated with the PD-related gut microbiome. Pathway enrichment analysis was then conducted on selected metabolite features from the PLS model.</div></div><div><h3>Results</h3><div>We identified 266 metabolite features and annotated 29 metabolic compounds associated with PD-related microbes (<em>p</em> &lt; 0.1). Enrichment analysis revealed perturbed pathways in lipid metabolism, including fatty acid activation and metabolism, linoleate metabolism, and glycerophospholipid metabolism, as well as carbohydrate metabolism such as hexose phosphorylation and starch/sucrose metabolism.</div></div><div><h3>Conclusion</h3><div>Our multi-omics integration analysis revealed that PD-associated gut microbiota are involved in host lipid metabolism, immune-related pathways, and potentially vitamin B-mediated regulation of kynurenine pathway metabolism, providing insights into potential microbiome–metabolome interactions in PD pathophysiology.</div></div>","PeriodicalId":72447,"journal":{"name":"Brain disorders (Amsterdam, Netherlands)","volume":"21 ","pages":"Article 100310"},"PeriodicalIF":0.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147421366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}