Differential Tractography: A Biomarker for Neuronal Function in Neurodegenerative Disease

Connor J Lewis, Zeynep Vardar, Anna Luisa Kühn, Jean M Johnston, Precilla D'Souza, William A Gahl, Mohammed Salman Shazeeb, Cynthia J Tifft, Maria T Acosta
{"title":"Differential Tractography: A Biomarker for Neuronal Function in Neurodegenerative Disease","authors":"Connor J Lewis, Zeynep Vardar, Anna Luisa Kühn, Jean M Johnston, Precilla D'Souza, William A Gahl, Mohammed Salman Shazeeb, Cynthia J Tifft, Maria T Acosta","doi":"10.1101/2024.08.25.24312255","DOIUrl":null,"url":null,"abstract":"GM1 gangliosidosis is an ultra-rare inherited neurodegenerative lysosomal storage disorder caused by biallelic mutations in the <em>GLB1</em> gene. GM1 is uniformly fatal and has no approved therapies, although clinical trials investigating gene therapy as a potential treatment for this condition are underway. Novel outcome measures or biomarkers demonstrating the longitudinal effects of GM1 and potential recovery due to therapeutic intervention are urgently needed to establish efficacy of potential therapeutics. One promising tool is differential tractography, a novel imaging modality utilizing serial diffusion weighted imaging (DWI) to quantify longitudinal changes in white matter microstructure. In this study, we present the novel use of differential tractography in quantifying the progression of GM1 alongside age-matched neurotypical controls. We analyzed 113 DWI scans from 16 GM1 patients and 32 age-matched neurotypical controls to investigate longitudinal changes in white matter pathology. GM1 patients showed white matter degradation evident by both the number and size of fiber tract loss. In contrast, neurotypical controls showed longitudinal white matter improvements as evident by both the number and size of fiber tract growth. We also corroborated these findings by documenting significant correlations between cognitive global impression (CGI) scores of clinical presentations and our differential tractography derived metrics in our GM1 cohort. Specifically, GM1 patients who lost more neuronal fiber tracts also had a worse clinical presentation. This result demonstrates the importance of differential tractography as an important biomarker for disease progression in GM1 patients with potential extension to other neurodegenerative diseases and therapeutic intervention.","PeriodicalId":501375,"journal":{"name":"medRxiv - Genetic and Genomic Medicine","volume":"24 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"medRxiv - Genetic and Genomic Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1101/2024.08.25.24312255","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

GM1 gangliosidosis is an ultra-rare inherited neurodegenerative lysosomal storage disorder caused by biallelic mutations in the GLB1 gene. GM1 is uniformly fatal and has no approved therapies, although clinical trials investigating gene therapy as a potential treatment for this condition are underway. Novel outcome measures or biomarkers demonstrating the longitudinal effects of GM1 and potential recovery due to therapeutic intervention are urgently needed to establish efficacy of potential therapeutics. One promising tool is differential tractography, a novel imaging modality utilizing serial diffusion weighted imaging (DWI) to quantify longitudinal changes in white matter microstructure. In this study, we present the novel use of differential tractography in quantifying the progression of GM1 alongside age-matched neurotypical controls. We analyzed 113 DWI scans from 16 GM1 patients and 32 age-matched neurotypical controls to investigate longitudinal changes in white matter pathology. GM1 patients showed white matter degradation evident by both the number and size of fiber tract loss. In contrast, neurotypical controls showed longitudinal white matter improvements as evident by both the number and size of fiber tract growth. We also corroborated these findings by documenting significant correlations between cognitive global impression (CGI) scores of clinical presentations and our differential tractography derived metrics in our GM1 cohort. Specifically, GM1 patients who lost more neuronal fiber tracts also had a worse clinical presentation. This result demonstrates the importance of differential tractography as an important biomarker for disease progression in GM1 patients with potential extension to other neurodegenerative diseases and therapeutic intervention.
差异牵张成像:神经退行性疾病中神经元功能的生物标志物
GM1 神经节苷脂病是一种超罕见的遗传性神经退行性溶酶体贮积症,由 GLB1 基因的双倍突变引起。GM1神经节苷脂病是一种致命性疾病,目前还没有获得批准的治疗方法,但研究基因疗法作为一种潜在治疗方法的临床试验正在进行中。为了确定潜在疗法的疗效,迫切需要新的结果测量或生物标志物来证明 GM1 的纵向影响以及治疗干预可能带来的恢复。其中一种很有前景的工具是差异束成像,这是一种新型成像模式,利用序列扩散加权成像(DWI)量化白质微观结构的纵向变化。在本研究中,我们展示了利用差异束成像量化 GM1 与年龄匹配的神经典型对照组的进展的新方法。我们分析了来自 16 名 GM1 患者和 32 名年龄匹配的神经典型对照者的 113 张 DWI 扫描图像,以研究白质病理学的纵向变化。GM1患者的白质退化表现在纤维束缺失的数量和大小上。与此相反,神经典型对照组的白质纵向变化则表现为纤维束数量和大小的增长。我们还通过记录临床表现的认知总体印象(CGI)评分与我们的GM1队列中不同纤维束成像得出的指标之间的显著相关性来证实这些发现。具体来说,神经元纤维束丢失较多的 GM1 患者的临床表现也较差。这一结果表明了差异束成像作为 GM1 患者疾病进展的重要生物标志物的重要性,并有可能推广到其他神经退行性疾病和治疗干预中。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信