Pregnancy hormone repairs myelin damage in MS mouse model

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SUMMARY
Treating a mouse model of multiple sclerosis with the pregnancy hormone estriol reversed the breakdown of myelin in the brain’s cortex, a key region affected in multiple sclerosis, according to a new UCLA Health study.

BACKGROUND
In multiple sclerosis, inflammation spurs the immune system to strip away the protective myelin coating around nerve fibers in the brain’s cortex, hampering electrical signals sent and received by the brain. Atrophy of the cortex in MS patients is associated with permanent worsening of disability, such as cognitive decline, visual impairment, weakness and sensory loss.

No currently available treatments for MS can repair damage to myelin. Instead, these treatments target inflammation to reduce symptom flare-ups and new nerve tissue scarring. Previous UCLA-led research found that estriol, a type of estrogen hormone produced in pregnancy, reduced brain atrophy and improved cognitive function in MS patients.

FINDINGS
In the new study, researchers treated a mouse model of MS with estriol and found that it prevented brain atrophy and induced remyelination in the cortex, indicating that the treatment can repair damage caused by MS, rather than just slow the destruction of myelin.

IMPACT
This is the first study to identify a treatment that could repair myelin in the cortex, undoing some of the damage caused by MS.

JOURNAL
The study, “Neuroprotection in cerebral cortex induced by the pregnancy hormone estriol,” is published online in Laboratory Investigation.

Allan MacKenzie-Graham, an associate professor of neurology, is the study’s corresponding author. Other authors include Cassandra Meyer, Andrew Smith, Aitana A. Padilla-Requerey, Vista Farkhondeh, Noriko Itoh, Yuichiro Itoh, Josephine Gao, Patrick Herbig, Quynhanh Nguyen, Katelyn Ngo, Mandavi Oberoi, Prabha Siddarth and Rhonda R. Voskuhl, all of UCLA.

Dr. Voskhul is an inventor of UCLA patents pertaining to estriol and ERβ ligand treatments. Please see the study for funding information.

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