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Open Access Publications from the University of California

The Center for the Study of Neurodegenerative Disorders at the University of California, Santa Barbara is located within the Neuroscience Research Institute at UCSB. Our focus is to understand neurodegenerative disorders from many perspectives and to contribute to their effective treatment and management. Our emphasis is primarily on multiple sclerosis (MS) and other demyelinating disorders, though our approaches in technical development and integrative studies suggest our approaches may be helpful for a variety of disorders.

We seek to integrate new approaches in bioengineering and traditional medicines. How to solve a disease of unknown cause, inadequate treatment, and unpredictable course? That is what we hope to review and update on this website, our approaches. We learn as much as possible from those with MS. We also promote mentorship and have helped fill the need for pre-medical experiences at UCSB due to the lack of a medical school here. For eight years we have worked with local high schools and undergraduate pre-medical and/or biomedical research students.

The Center's Director, Dr. Cynthia Husted (, has a doctorate in the physical chemistry of myelin lipids from the University of Illinois Urbana-Champaign with an emphasis on the theory and instrumentation of nuclear magnetism and applications to myelin lipids and changes in development and disease. Postdoctoral studies were in neuroradiology at UCSF. She also worked as a registered nurse in the intensive care unit for 5 years, with hands-on medical experience. She has continued these interests during her career along with studies of traditional medicines, currently with an emphasis on Tibetan medicine, and other expansions into physical chemistry, such as Langmuir monolayers, fluorescence microscopy, atomic force microscopy, and calculations of myelin membrane forces. This website is an ongoing exploration of the merging of disciplines. Feedback is appreciated.

Myelin is a multi-lamellar membrane which functions as an insulator for conduction of nerve impulses. Multiple Sclerosis (MS) is considered an autoimmune disorder of the central nervous system and myelin is recognized as foreign and destroyed. Our research plan has two primary hypotheses:

  • Hypothesis 1: Inherent differences in myelin lipids from normal-appearing white matter (NAWM) contribute to the onset and progression of demyelination in MS.
  • Hypothesis 2: Myelin lipids are altered in acute immune-mediated demyelination in a manner that promotes demyelination.
Cover page of Sphingomyelin-cholesterol superlattices as detected with Langmuir isotherms: their potential role in myelin and demyelination

Sphingomyelin-cholesterol superlattices as detected with Langmuir isotherms: their potential role in myelin and demyelination


ABSTRACT In Multiple Sclerosis (MS) and Experimental Allergic Encephalomyelitis (EAE) in the common marmoset, demyelination appears to result from loss of adhesion between adjacent myelin lamellae and the formation of small myelin vesicles. Although proteins are involved in maintaining normal myelin structure, lipids may play an essential role in myelin stability. In the current study we focused on the effect that disturbed ratios of sphingomyelin (SM) and cholesterol may have on the regular distribution of those molecules. Mixtures of egg SMs (saturated) and bovine brain SMs (partially unsaturated) with cholesterol were made and examined with Langmuir isotherms. The cholesterol-induced condensations of the average molecular areas were determined by classic mean molecular area vs. composition plots. The results showed that egg SMs are significantly more expanded than bovine brain SMs, contrary to the fact that they are more saturated. We believe this is due to the fact that two-dimensional phase transitions of the predominant acyl chain species of egg SM generally occur at lower pressures compared to the predominant species in bovine brain SM due to their shorter acyl chain lengths. Furthermore we found that just beyond 22.2 mol% cholesterol, a predicted superlattice concentration, the condensation effect of cholesterol dramatically increases. We explain this by the fact that just beyond this point, the membrane regions containing only SM molecules have completely disappeared.