Ropper AH, Samuels MA, Klein J. Adams and Victor’s principles of neurology. Eleventh. New York: McGraw-Hill Education; 2019.
Wallin MT, et al. The prevalence of MS in the United States: A population-based estimate using health claims data. Neurol. 2019;92(10):e1029–40. https://doi.org/10.1212/WNL.0000000000007035.
Kuhlmann T, et al. Multiple sclerosis progression: time for a new mechanism-driven framework. Lancet Neurol. 2023;22(1):78–88. https://doi.org/10.1016/S1474-4422(22)00289-7.
Stankoff B, et al. Age at onset determines the occurrence of the progressive phase of multiple sclerosis. Neurol. 2007;68(10):779–81. https://doi.org/10.1212/01.wnl.0000256732.36565.4a.
M. P. Gorman, B. C. Healy, M. Polgar-Turcsanyi, and T. Chitnis, “Increased Relapse Rate in Pediatric-Onset Compared With Adult-Onset Multiple Sclerosis,” Arch. Neurol., vol. 66, no. 1, 2009, https://doi.org/10.1001/archneurol.2008.505.
Scalfari A, Neuhaus A, Daumer M, Ebers GC, Muraro PA. Age and disability accumulation in multiple sclerosis. Neurology. 2011;77(13):1246–52. https://doi.org/10.1212/WNL.0b013e318230a17d.
Article CAS PubMed PubMed Central Google Scholar
Harding KE, et al. Long-term outcome of paediatric-onset multiple sclerosis: a population-based study. J Neurol Neurosurg Psychiatry. 2013;84(2):141–7. https://doi.org/10.1136/jnnp-2012-303996.
Tutuncu M, et al. Onset of progressive phase is an age-dependent clinical milestone in multiple sclerosis. Mult Scler J. 2013;19(2):188–98. https://doi.org/10.1177/1352458512451510.
E. Waubant et al., “Difference in Disease Burden and Activity in Pediatric Patients on Brain Magnetic Resonance Imaging at Time of Multiple Sclerosis Onset vs Adults,” Arch Neurol., vol. 66, no. 8, 2009, https://doi.org/10.1001/archneurol.2009.135.
Pfeifenbring S, et al. Extensive acute axonal damage in pediatric multiple sclerosis lesions. Ann Neurol. 2015;77(4):655–67. https://doi.org/10.1002/ana.24364.
Article CAS PubMed PubMed Central Google Scholar
Tremlett H, Zhao Y, Joseph J, Devonshire V, the UBCMS Clinic Neurologists. 2“Relapses in multiple sclerosis are age- and time-dependent.” J Neurol Neurosurg Psychiatry. 2008;79(12):1368–74. https://doi.org/10.1136/jnnp.2008.14580.
Article CAS PubMed Google Scholar
Lucchinetti C, Bruck W, Parisi J, Scheithauer B, Rodriguez M, Lassmann H. Heterogeneity of multiple sclerosis lesions: Implications for the pathogenesis of demyelination. Ann Neurol. 2000;47(6):707–17. https://doi.org/10.1002/1531-8249(200006)47:6%3c707::AID-ANA3%3e3.0.CO;2-Q.
Article CAS PubMed Google Scholar
Frischer JM, et al. Clinical and pathological insights into the dynamic nature of the white matter multiple sclerosis plaque. Ann Neurol. 2015;78(5):710–21. https://doi.org/10.1002/ana.24497.
Article PubMed PubMed Central Google Scholar
Jäckle K, et al. Molecular signature of slowly expanding lesions in progressive multiple sclerosis. Brain. 2020;143(7):2073–88. https://doi.org/10.1093/brain/awaa158.
• M. Absinta et al., “A lymphocyte–microglia–astrocyte axis in chronic active multiple sclerosis,” Nature, vol. 597, no. 7878, pp. 709–714, 2021https://doi.org/10.1038/s41586-021-03892-7This study describes a genetic profile of disease associated microglia in MS.
Nicaise AM, et al. Cellular senescence in progenitor cells contributes to diminished remyelination potential in progressive multiple sclerosis. Proc Natl Acad Sci. 2019;116(18):9030–9. https://doi.org/10.1073/pnas.1818348116.
Article ADS CAS PubMed PubMed Central Google Scholar
• A. Calvi et al., “Relationship between paramagnetic rim lesions and slowly expanding lesions in multiple sclerosis,” Mult Scler J., vol. 29, no. 3, pp. 352–362, Mar. 2023https://doi.org/10.1177/13524585221141964This study describes paramagnetic rim and slowly expanding lesions in multiple sclerosis and reports association with progression.•
Elliott C, et al. Chronic white matter lesion activity predicts clinical progression in primary progressive multiple sclerosis. Brain. 2019;142(9):2787–99. https://doi.org/10.1093/brain/awz212.
Article PubMed PubMed Central Google Scholar
P. Maggi et al., “Chronic White Matter Inflammation and Serum Neurofilament Levels in Multiple Sclerosis,” Neurology, vol. 97, no. 6, 2021, https://doi.org/10.1212/WNL.0000000000012326.
Absinta M, et al. Association of Chronic Active Multiple Sclerosis Lesions With Disability In Vivo. JAMA Neurol. 2019;76(12):1474. https://doi.org/10.1001/jamaneurol.2019.2399.
Article PubMed PubMed Central Google Scholar
Absinta M, et al. Persistent 7-tesla phase rim predicts poor outcome in new multiple sclerosis patient lesions. J Clin Invest. 2016;126(7):2597–609. https://doi.org/10.1172/JCI86198.
Article PubMed PubMed Central Google Scholar
Vollmer T, et al. The natural history of brain volume loss among patients with multiple sclerosis: A systematic literature review and meta-analysis. J Neurol Sci. 2015;357(1–2):8–18. https://doi.org/10.1016/j.jns.2015.07.014.
Azevedo CJ, Cen SY, Jaberzadeh A, Zheng L, Hauser SL, Pelletier D. Contribution of normal aging to brain atrophy in MS. Neurol Neuroimmunol Neuroinflammation. 2019;6(6): e616. https://doi.org/10.1212/NXI.0000000000000616.
Zhang J, et al. Gray matter atrophy cannot be fully explained by white matter damage in patients with MS. Mult Scler J. 2021;27(1):39–51. https://doi.org/10.1177/1352458519900972.
M. A. Rocca et al., “Association of Gray Matter Atrophy Patterns With Clinical Phenotype and Progression in Multiple Sclerosis,” Neurology, vol. 96, no. 11, 2021, https://doi.org/10.1212/WNL.0000000000011494.
Bø L, Vedeler CA, Nyland HI, Trapp BD, Mørk SJ. Subpial Demyelination in the Cerebral Cortex of Multiple Sclerosis Patients. J Neuropathol Exp Neurol. 2003;62(7):723–32. https://doi.org/10.1093/jnen/62.7.723.
Bell L, Lenhart A, Rosenwald A, Monoranu CM, Berberich-Siebelt F. Lymphoid Aggregates in the CNS of Progressive Multiple Sclerosis Patients Lack Regulatory T Cells. Front Immunol. 2020;10:3090. https://doi.org/10.3389/fimmu.2019.03090.
Article CAS PubMed PubMed Central Google Scholar
Van Olst L, et al. Meningeal inflammation in multiple sclerosis induces phenotypic changes in cortical microglia that differentially associate with neurodegeneration. Acta Neuropathol (Berl). 2021;141(6):881–99. https://doi.org/10.1007/s00401-021-02293-4.
Article CAS PubMed Google Scholar
Levine ME. Modeling the Rate of Senescence: Can Estimated Biological Age Predict Mortality More Accurately Than Chronological Age? J Gerontol A Biol Sci Med Sci. 2013;68(6):667–74. https://doi.org/10.1093/gerona/gls233.
Blackburn EH, Epel ES, Lin J. Human telomere biology: A contributory and interactive factor in aging, disease risks, and protection. Science. 2015;350(6265):1193–8. https://doi.org/10.1126/science.aab3389.
Article ADS CAS PubMed Google Scholar
Krysko KM, et al. Telomere Length Is Associated with Disability Progression in Multiple Sclerosis. Ann Neurol. 2019;86(5):671–82. https://doi.org/10.1002/ana.25592.
Article CAS PubMed PubMed Central Google Scholar
Musella A, et al. Interplay Between Age and Neuroinflammation in Multiple Sclerosis: Effects on Motor and Cognitive Functions. Front Aging Neurosci. 2018;10:238. https://doi.org/10.3389/fnagi.2018.00238.
Article CAS PubMed PubMed Central Google Scholar
R. G. Morgan, A. J. Donato, and A. E. Walker, “Telomere uncapping and vascular aging,” Am J Physiol-Heart Circ Physiol., vol. 315, no. 1, pp. H1–H5, 2018, https://doi.org/10.1152/ajpheart.00008.2018.
M. A. Giardini, M. Segatto, M. S. Da Silva, V. S. Nunes, and M. I. N. Cano, “Telomere and Telomerase Biology,” in Progress in Molecular Biology and Translational Science, vol. 125, Elsevier, 2014, pp. 1–40. https://doi.org/10.1016/B978-0-12-397898-1.00001-3.
Goglin SE, Farzaneh-Far R, Epel ES, Lin J, Blackburn EH, Whooley MA. Change in Leukocyte Telomere Length Predicts Mortality in Patients with Stable Coronary Heart Disease from the Heart and Soul Study. PLoS ONE. 2016;11(10): e0160748. https://doi.org/10.1371/journal.pone.0160748.
Article CAS PubMed PubMed Central Google Scholar
Willeit P, et al. Cellular Aging Reflected by Leukocyte Telomere Length Predicts Advanced Atherosclerosis and Cardiovascular Disease Risk. Arterioscler Thromb Vasc Biol. 2010;30(8):1649–56. https://doi.org/10.1161/ATVBAHA.110.205492.
Article CAS PubMed Google Scholar
Topiwala A, et al. Alcohol consumption and telomere length: Mendelian randomization clarifies alcohol’s effects. Mol Psychiatry. 2022;27(10):4001–8. https://doi.org/10.1038/s41380-022-01690-9.
Article CAS PubMed PubMed Central Google Scholar
Galiè S, Canudas S, Muralidharan J, García-Gavilán J, Bulló M, Salas-Salvadó J. Impact of Nutrition on Telomere Health: Systematic Review of Observational Cohort Studies and Randomized Clinical Trials. Adv Nutr. 2020;11(3):576–601. https://doi.org/10.1093/advances/nmz107.
Song S, Lee E, Kim H. Does Exercise Affect Telomere Length? A Systematic Review and Meta-Analysis of Randomized Controlled Trials. Medicina (Mex). 2022;58(2):242. https://doi.org/10.3390/medicina58020242.
Khosravaniardakani S, et al. Obesity Accelerates Leukocyte Telomere Length Shortening in Apparently Healthy Adults: A Meta-Analysis. Front Nutr. 2022;9: 812846. https://doi.org/10.3389/fnut.2022.812846.
Article PubMed PubMed Central Google Scholar
Astuti Y, Wardhana A, Watkins J, Wulaningsih W. Cigarette smoking and telomere length: A systematic review of 84 studies and meta-analysis. Environ Res. 2017;158:480–9.
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