ASN NEURO最新文献

{"title":"Demystifying The Myelin <i>g</i> Ratio: Its Origin, Derivation and Interpretation.","authors":"Alexander Gow","doi":"10.1080/17590914.2025.2542166","DOIUrl":"10.1080/17590914.2025.2542166","url":null,"abstract":"<p><p>Most studies involving myelin <i>g</i> ratios over the past 120 years assume this metric enumerates differences in myelin thickness (larger <i>g</i> ratio = thinner myelin) with axon or fiber diameter. And, moreover, such changes are directly correlated with internodal function (conduction velocity). However, such assumptions are warranted only in the absence of experimental errors and artifacts (i.e. under theoretical conditions). In reality, <i>g</i> ratios can easily under- or overestimate the rate of change for this relation in excess of 10%, especially for small caliber fibers. Typical analyses of myelin internodes rely on an explicit mathematical model, <math><mi>g</mi><mi> </mi><mtext>ratio</mtext><mo>=</mo><mrow><mfrac><mrow><mrow><msub><mrow><mi>D</mi></mrow><mrow><mi>A</mi></mrow></msub></mrow></mrow><mrow><mrow><msub><mrow><mi>D</mi></mrow><mrow><mi>F</mi></mrow></msub></mrow></mrow></mfrac></mrow><mtext>,</mtext></math> where D_A is axon diameter and D_F is fiber diameter (myelin plus axon). Shown recently and herein, this model approximates normal physiological conditions only when the axon-fiber diameter relation is directly proportional, whence it is concordant with the axomyelin unit model. However, in transient or non-steady states (development/aging, disease or myelin plasticity) with linear but not directly proportional relations, <i>g</i> ratios may not accurately describe myelin structure. Acceptance of this counterintuitive assertion is predicated on a detailed understanding of the <i>g</i> ratio - its origins, properties and the biology represented - which has been heretofore unexplored. In light of such <i>g</i> ratio limitations, and toward consistency with experimental data, two more reliable metrics are proposed, the myelin <i>g_c</i> ratio and the <i>g'</i> cline. But irrespective which of metric is preferred , the analysis herein shows that the axon-to-fiber diameter ratio under normal physiological conditions is a constant for all fiber diameters.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2542166"},"PeriodicalIF":3.7,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12360196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862091","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Understanding the Myelin <i>g</i> Ratio from First Principles, Its Derivation, Uses and Artifacts.","authors":"Alexander Gow","doi":"10.1080/17590914.2024.2445624","DOIUrl":"10.1080/17590914.2024.2445624","url":null,"abstract":"<p><p>In light of the increasing importance for measuring myelin <i>g</i> ratios - the ratio of axon-to-fiber (axon + myelin) diameters in myelin internodes - to understand normal physiology, disease states, repair mechanisms and myelin plasticity, there is urgent need to minimize processing and statistical artifacts in current methodologies. Many contemporary studies fall prey to a variety of artifacts, reducing study outcome robustness and slowing development of novel therapeutics. Underlying causes stem from a lack of understanding of the myelin <i>g</i> ratio, which has persisted more than a century. An extended exploratory data analysis from first principles (the axon-fiber diameter relation) is presented herein and has major consequences for interpreting published <i>g</i> ratio studies. Indeed, a model of the myelin internode naturally emerges because of (1) the strong positive correlation between axon and fiber diameters and (2) the demonstration that the relation between these variables is one of direct proportionality. From this model, a robust framework for data analysis, interpretation and understanding allows specific predictions about myelin internode structure under normal physiological conditions. Further, the model establishes that a regression fit to <i>g</i> ratio plots has zero slope, and it identifies the underlying causes of several data processing artifacts that can be mitigated by plotting <i>g</i> ratios against fiber diameter (not axon diameter). Hypothesis testing can then be used for extending the model and evaluating myelin internodal properties under pathophysiological conditions (forthcoming). For without a statistical model as anchor, hypothesis testing is aimless like a rudderless ship on the ocean.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2445624"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143031981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Statistically-Robust Model of the Axomyelin Unit under Normal Physiologic Conditions with Application to Disease States.","authors":"Alexander Gow, Jeffrey L Dupree, Douglas L Feinstein, Anne Boullerne","doi":"10.1080/17590914.2024.2447336","DOIUrl":"10.1080/17590914.2024.2447336","url":null,"abstract":"<p><p>Despite tremendous progress in characterizing the myriad cellular structures in the nervous system, a full appreciation of the interdependent and intricate interactions between these structures is as yet unfulfilled. Indeed, few more so than the interaction between the myelin internode and its ensheathed axon. More than a half-century after the ultrastructural characterization of this axomyelin unit, we lack a reliable understanding of the physiological properties, the significance and consequence of pathobiological processes, and the means to gauge success or failure of interventions designed to mitigate disease. Herein, we highlight shortcomings in the most common statistical procedures used to characterize the myelin <i>g</i> ratio, with particular emphasis on the underlying principles of simple linear regression. These shortcomings lead to insensitive detection and/or ambiguous interpretation of normal physiology, disease mechanisms and remedial methodologies. To address these problems, we syndicate insights from early seminal myelin studies and use a statistical model of the axomyelin unit that is established in Gow (2025). Herein, we develop and demonstrate a statistically-robust analysis pipeline with which to examine and interpret axomyelin physiology and pathobiology in two disease states, experimental autoimmune encephalomyelitis and the <i>rumpshaker</i> mouse model of leukodystrophy. On a cautionary note, our pipeline is a relatively simple and streamlined approach that is not necessarily a panacea for all <i>g</i> ratio analyses. Rather, it approximates a minimum effort needed to elucidate departures from normal physiology and to determine if more comprehensive studies may lead to deeper insights.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2447336"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11974466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143063471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Analysis of Oligodendrocyte Lineage Cell Progression with Cre-Mediated RiboTag Reporter Lines.","authors":"George S Melchor, Maya S Shah, Zeeba Manavi, Lauren M Rosko, Jingwen Hu, Haiyang Wang, Maryna Baydyuk, Jeffrey K Huang","doi":"10.1080/17590914.2025.2513885","DOIUrl":"10.1080/17590914.2025.2513885","url":null,"abstract":"<p><p>Cre-reporter strategies in transgenic mice are widely used to assess the specificity of gene promoter activities, and for fate-mapping studies during development and under injury conditions. The ribosome tagging strategy, RiboTag, is a transgenic approach, in which a hemagglutinin (HA) tag fused to the endogenous ribosomal protein, RPL22, is expressed through the Cre/loxP system. To profile RiboTag reporter expression in oligodendrocyte lineage cells (OLCs), we generated NG2^Cre:Rpl22^HA, Pdgfra^CreERT:Rpl22^HA, and Plp^CreERT:Rpl22^HA mice. We found that NG2^Cre:Rpl22^HA displayed strong HA reporter expression in OLCs and neuronal subpopulations in the postnatal CNS. Tamoxifen administration into Pdgfra^CreERT:Rpl22^HA and Plp^CreERT:Rpl22^HA mice led to widespread HA reporter expression in oligodendrocyte precursor cells (OPCs) and oligodendrocytes, respectively, throughout the brain and spinal cord. Following focal demyelinating injury, Pdgfra^CreERT:Rpl22^HA mice exhibited HA labeling in OPCs, with a gradual increase in oligodendrocyte labeling during remyelination. In contrast, Plp^CreERT:Rpl22^HA exhibited oligodendrocyte labeling in lesions and throughout the CNS parenchyma, presenting a challenge in distinguishing newly generated oligodendrocytes during remyelination from pre-existing oligodendrocytes. Notably, HA expression was induced in oligodendrocytes, but not OPCs in demyelinated lesions of Plp^CreERT:Rpl22^HA mice even when the demyelinating injury was conducted several days after tamoxifen had cleared. This suggests a potential regulation of gene expression in OPCs in demyelinated lesions, in which Rpl22^HA translation may be prevented until oligodendrocyte differentiation occurs. Overall, the RiboTag reporter demonstrates high sensitivity and stability, and its potential application should be carefully considered in relation to the experimental model, timeline in which it will be used, and cell tracking conditions.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2513885"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12169044/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Brain Endothelial Cell Caveolin-1/CXCL10 Axis Promotes T Cell Transcellular Migration Across the Blood-Brain Barrier.","authors":"Troy N Trevino, Ali A Almousawi, Remy Martins-Goncalves, Andrea Ochoa-Raya, KaReisha F Robinson, Genesis L Abad, Leon M Tai, Suellen D Oliveira, Richard D Minshall, Sarah E Lutz","doi":"10.1080/17590914.2025.2472070","DOIUrl":"10.1080/17590914.2025.2472070","url":null,"abstract":"<p><p>The mechanisms that govern whether T cells cross blood-brain barrier (BBB) endothelium by transcellular versus paracellular routes are unclear. Caveolin-1 is a membrane scaffolding and signaling protein associated with transcellular transmigration through the endothelial cytoplasm. Here, we report that the neuroinflammatory chemokine CXCL10 induced transcellular, caveolar transmigration of CXCR3+ CD4+ T cells. Specifically, data revealed that CXCL10-induced transcellular transmigration requires expression of Caveolin-1 and ICAM-1 in brain endothelial cells and of the CXCL10 receptor, CXCR3, and LFA-1 in T cells. Moreover, Caveolin-1 promoted CXCL10 aggregation into brain endothelial cytoplasmic stores, providing a mechanism for activation and recruitment of CXCR3+ T cells to migrate at cytoplasmic locations, distal to cell-cell junctions. Consistent with our <i>in vitro</i> data, genetic ablation of Caveolin-1 reduces infiltration of CXCR3+ CD4+ T cells into the CNS in experimental autoimmune encephalomyelitis. Our findings establish a novel mechanism by which brain endothelial cells utilize Caveolin-1 dependent CXCL10 intracellular stores to license T cells for transcellular migration across the blood-brain barrier.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2472070"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12047051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex Affects Cognitive Outcomes in HIV-1 Tat Transgenic Mice: Role of CCR5.","authors":"Chloe A Simons, Sarah Kim, Yun K Hahn, Ama Boake-Agyei, Sara R Nass, Phu Vo, Kurt F Hauser, Pamela E Knapp","doi":"10.1080/17590914.2024.2447338","DOIUrl":"10.1080/17590914.2024.2447338","url":null,"abstract":"<p><p>People living with HIV (PLWH) experience HIV-associated neurocognitive disorders (HAND), even though combination antiretroviral therapy (cART) suppresses HIV replication. HIV-1 transactivator of transcription (HIV-1 Tat) contributes to the development of HAND through neuroinflammatory and neurotoxic mechanisms. C-C chemokine 5 receptor (CCR5) is important in immune cell targeting and is a co-receptor for HIV viral entry into CD4+ cells. Notably, CCR5 has been implicated in cognition unrelated to HIV infection. Inhibition of CCR5 has been shown to improve learning and memory. To test whether CCR5 is involved in cognitive changes in HAND, we used a non-infectious, transgenic model in which HIV-1 Tat is inducibly expressed. Well-powered cohorts of male and female mice were placed on a diet containing doxycycline to induce Tat expression for 8-wks. Males showed Tat-mediated deficits in the Barnes maze test of spatial learning and memory; females showed no impairments. Deficits in the males were fully reversed by the CCR5 antagonist, maraviroc (MVC). Tat-mediated deficits were not found in novel object recognition or contextual fear conditioning in either sex. Based on earlier work, we hypothesized that MVC might increase brain-derived neurotrophic factor (BDNF), which is essential in maintaining synaptodendritic function. MVC did increase the mBDNF to proBDNF ratio in males, perhaps contributing to improved cognition.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2447338"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11877617/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142977399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"P-glycoprotein and Alzheimer's Disease: Threats and Opportunities.","authors":"Joseph Jr Asante, Steven W Barger","doi":"10.1080/17590914.2025.2495632","DOIUrl":"10.1080/17590914.2025.2495632","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder that affects more than 50 million people worldwide. One of the hallmark features of AD is the accumulation of amyloid β-peptide (Aβ) protein in the brain. P-glycoprotein (P-gp) is a membrane-bound protein expressed in various tissues, including the cerebrovascular endothelium. It plays a crucial role in the efflux of toxic substances, including Aβ, from the brain. Aberrations in P-gp levels or activity have been implicated in the pathogenesis of AD by promoting the accumulation of Aβ in the brain. Therefore, modulating the P-gp function represents a promising therapeutic strategy for treating AD. P-gp has multiple substrate binding sites, creating the potential for substrates to fall into complementation groups based on these sites; two substrates in the same complementation group may compete with one other, but two substrates in different groups may exhibit cooperativity. Thus, a given P-gp substrate may interfere with Aβ efflux whereas another may promote clearance. These threats and opportunities, as well as other aspects of P-gp relevance to AD, are discussed here.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2495632"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proliferating Microglia Exhibit Unique Transcriptional and Functional Alterations in Alzheimer's Disease.","authors":"Nàdia Villacampa, Heela Sarlus, Paula Martorell, Khushbu Bhalla, Sergio Castro-Gomez, Ana Vieira-Saecker, Ilya Slutzkin, Kristian Händler, Carmen Venegas, Róisín McManus, Thomas Ulas, Marc Beyer, Eran Segal, Michael T Heneka","doi":"10.1080/17590914.2025.2506406","DOIUrl":"10.1080/17590914.2025.2506406","url":null,"abstract":"<p><p>Proliferation of microglia represents a physiological process, which is accelerated in several neurodegenerative disorders including Alzheimer disease (AD). The effect of such neurodegeneration-associated microglial proliferation on function and disease progression remains unclear. Here, we show that proliferation results in profound alterations of cellular function by providing evidence that newly proliferated microglia show impaired beta-amyloid clearance in vivo. Through sorting of proliferating microglia of APP/PS1 mice and subsequent transcriptome analysis, we define unique proliferation-associated transcriptomic signatures that change with age and beta-amyloid accumulation and are characterized by enrichment of immune system-related pathways. Of note, we identify the DEAD-Box Helicase 3 X-Linked (DDX3X) as a key molecule to modulate microglia activation and cytokine secretion and it is expressed in the AD brain. Together, these results argue for a novel concept by which phenotypic and functional microglial changes occur longitudinally as a response to accelerated proliferation in a neurodegenerative environment.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2506406"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144092761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined Treatment with Minocycline and an mGluR5 Antagonist Alters Resting EEG Spectral Power, but Not Sound-Evoked Responses, in a Mouse Model of Fragile X Syndrome.","authors":"M H Kassir, J W Lovelace, D K Binder, I E Ethell, K A Razak","doi":"10.1080/17590914.2025.2564628","DOIUrl":"https://doi.org/10.1080/17590914.2025.2564628","url":null,"abstract":"<p><p>Fragile X Syndrome (FXS) is a leading genetic cause of intellectual disability and autism-like behaviors. Glutamatergic mGluR5 receptors and matrix metalloproteinase-9 (MMP-9) are therapeutic targets to treat FXS, but clinical trials targeting each of these pathways have not been successful. Here, we tested if the electroencephalography (EEG) phenotypes associated with FXS are reversed with a novel combination of treatments affecting the two pathways. <i>Fmr1</i> knockout (KO) mice were given 10 days of CTEP (mGluR5 antagonist) alone or in combination with minocycline (MMP-9 inhibitor). EEG was recorded during resting (no acoustic stimulation) and during sound presentations (to produce sound-evoked EEG) at 1 day and 10 days after the beginning of treatment administration to test acute effects and potential tachyphylaxis. In pre-treatment WT and KO mice comparisons, we replicated previously published <i>Fmr1</i> KO mouse EEG phenotypes including elevated power in the resting gamma band, elevated single trial power, and reduced phase-locking to spectrotemporally dynamic auditory stimuli. We found that CTEP treatment alone did not show any benefit compared to vehicle in <i>Fmr1</i> KO mice after either 1 or 10 days of treatment. CTEP + minocycline reduced resting gamma band power in the <i>Fmr1</i> KO mice to a greater extent than vehicle at both treatment time points. There were no effects on sound-evoked responses. These data suggest that combined CTEP and minocycline treatment alters resting EEG measures while each treatment administered separately does not yield similar changes. High power in broadband gamma frequency correlates with irritability, stereotyped behaviors, and hyperactivity in FXS patients, suggesting a combination of drugs that reduce mGluR5 and MMP-9 activity may be beneficial in FXS.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2564628"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145298505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying Lanthionine Ketimine Derivatives for Maturation and Proliferative Effects in Oligodendrocyte Progenitor Cells.","authors":"Zachary McDonald, Ankit Tandon, Travis T Denton, Mehek Taneja, Jacqueline Rocha, Jeffrey L Dupree, Pablo M Paez, Veronica T Cheli, Swathi G Tumuluri, Douglas L Feinstein","doi":"10.1080/17590914.2025.2535963","DOIUrl":"10.1080/17590914.2025.2535963","url":null,"abstract":"<p><p>Previous studies have shown that lanthionine ketimine ethyl ester (LKE) reduces clinical scores in the experimental autoimmune encephalomyelitis (EAE) mouse model of Multiple Sclerosis, induces differentiation of oligodendrocyte progenitor cells (OPCs) in vitro, and accelerates remyelination following cuprizone induced demyelination. In a search for derivatives with greater efficacy to induce OPC maturation or proliferation, we screened a panel of 2-alkyl and 3-phosphonate substituted LK derivatives. Incubation of Oli-neu oligodendrocyte cells with 2-<i>n</i>-butyl- or 2-<i>n</i>-hexyl-LKE-phosphonate reduced spontaneous cell death, increased proliferation, and increased maturation. These were associated with changes in corresponding mRNA levels of Olig2, PLP, and O4. These derivatives also reduced cell death and increased proliferation and maturation in primary mouse OPCs. The increased hydrophobicity of these derivatives suggests these will be better candidates for testing effects in animal models of Multiple Sclerosis and other demyelinating diseases.</p>","PeriodicalId":8616,"journal":{"name":"ASN NEURO","volume":"17 1","pages":"2535963"},"PeriodicalIF":3.7,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296138/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144681923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}