Jaftha Mariaan, Robertson Frances, van Rensburg Susan J, Kidd Martin, van Toorn Ronald, Kemp Merlisa C, Johannes Clint, Moremi Kelebogile E, Whati Lindiwe, Kotze Maritha J, Engel-Hills Penelope
Department of Medical Imaging and Therapeutic Sciences, Faculty of Health and Wellness Sciences, Cape Peninsula University of Technology, Bellville, Cape Town, South Africa.
Cape University Body Imaging Centre, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.
Mult Scler Int. 2024 Nov 1;2024:8818934. doi: 10.1155/2024/8818934. eCollection 2024.
: Cerebral white matter lesion (WML) formation in people with multiple sclerosis (pwMS) is linked to the death of myelin-producing oligodendrocytes. Current MS treatment strategies focus on limiting WML accumulation and disability. Using a pathology-supported genetic testing (PSGT) program, we identified specific risk factors for MS, categorized as and . We developed a novel clinical methodology to mitigate these risk factors, including personalized lifestyle interventions and optimization of cerebral nutrients to prevent oligodendrocyte demise and promote remyelination. : To conduct a pilot case-control study over a 10-year period to ascertain whether the PSGT Program can reduce or prevent WML formation in pwMS. : MRI was performed at baseline as well as after an interval period of at least 10 years or longer in 22 pwMS. WML volumes were determined using Sequence Adaptive Multimodal SEGmentation (SAMSEG) software, part of FreeSurfer 7.2. Other variables included age at MRI, disease duration, disability status, and medication. : PwMS ( = 13) who had followed the PSGT program for more than 10 years, had significantly smaller lesion volumes (mm) compared to pwMS who did not adhere to the program ( = 9) (4950 ± 5303 vs. 17934 ± 11139; = 0.002). WML volumes were significantly associated ( = 0.02) with disability (EDSS) but not with age ( = 0.350), disease duration ( = 0.709), or Interferon- treatment ( = 0.70). Dietary and lifestyle changes may lower the risk of developing cerebral WMLs in pwMS and potentially slow disease progression. Larger studies are required to confirm the effectiveness of such interventions in pwMS.
多发性硬化症患者(pwMS)的脑白质病变(WML)形成与产生髓磷脂的少突胶质细胞死亡有关。目前的MS治疗策略侧重于限制WML积累和残疾。通过一项病理学支持的基因检测(PSGT)计划,我们确定了MS的特定风险因素,分为[具体类别未给出]和[具体类别未给出]。我们开发了一种新的临床方法来减轻这些风险因素,包括个性化生活方式干预和优化脑营养,以防止少突胶质细胞死亡并促进髓鞘再生。:进行一项为期10年的试点病例对照研究,以确定PSGT计划是否可以减少或预防pwMS中的WML形成。:对22名pwMS在基线以及至少10年或更长的间隔期后进行了MRI检查。使用FreeSurfer 7.2的一部分序列自适应多模态分割(SAMSEG)软件确定WML体积。其他变量包括MRI时的年龄、疾病持续时间、残疾状态和药物治疗。:遵循PSGT计划超过10年的pwMS(n = 13)与未遵循该计划的pwMS(n = 9)相比,病变体积(mm)明显更小(4950±5303 vs. 17934±11139;p = 0.002)。WML体积与残疾(EDSS)显著相关(p = 0.02),但与年龄(p = 0.350)、疾病持续时间(p = 0.709)或干扰素治疗(p = 0.70)无关。饮食和生活方式的改变可能会降低pwMS发生脑WML的风险,并可能减缓疾病进展。需要更大规模的研究来证实此类干预措施在pwMS中的有效性。