A stroke drug may help preserve and repair myelin damaged by multiple sclerosis, according to a review of animal studies.
Nimodipine was also linked to reduced inflammation, nerve damage and disease severity in several of the studies reviewed.
Myelin is the protective coating around nerve fibres that is damaged in multiple sclerosis, or MS, disrupting communication between the brain and the rest of the body.
Researchers in Iran reviewed five animal studies investigating whether nimodipine, a prescription medicine used to prevent blood vessel spasms after bleeding in the brain, could have potential as an MS treatment.
In MS, the immune system mistakenly attacks the myelin sheath, causing inflammation and nerve damage that can lead to a wide range of neurological symptoms.
Most current MS treatments work by modifying the immune system. While they can reduce relapses and slow disease progression, they generally do not directly repair myelin that has already been lost.
Nimodipine works by relaxing narrowed blood vessels to improve blood flow to injured brain tissue.
Previous research has suggested that the drug may also reduce inflammation and nerve damage while supporting myelin repair.
Four of the five studies involved rodents with experimental autoimmune encephalomyelitis, or EAE, a condition commonly used to model MS.
The fifth used cuprizone, a toxin that causes demyelination, meaning the loss of the protective myelin coating around nerves.
The studies differed substantially in the animals and disease models used, nimodipine doses, treatment methods and outcome measures, so researchers could not combine the results into a single statistical analysis.
Instead, they carried out a narrative review of the results.
Overall, nimodipine was linked to reduced disease severity in the EAE models.
One study found that the drug reduced the severity of relapsing-remitting EAE and lessened disease severity during the early active phase.
Other studies reported reduced relapse rates, fewer sensory and motor problems and effects suggesting protection of nerve cells.
Nimodipine was also linked to less myelin loss and fewer demyelinated nerve fibres.
In one study, treatment increased the number of nerve fibres showing signs of remyelination, the process through which damaged myelin is rebuilt.
The findings were accompanied by increased activity in genes linked to myelin and higher numbers of cells involved in myelin regeneration.
Animals treated with nimodipine also showed fewer signs of inflammation in the brain and spinal cord and lower blood levels of some inflammation-related proteins.
The drug was also linked to improved blood flow and oxygen levels in the spinal cord, while one study found reduced clinical scores and improved motor performance.
In the cuprizone model, nimodipine was linked to fewer reactive immune cells in the brain and faster, more complete myelin repair.
The researchers called for further studies to reproduce the findings and early-stage human trials to determine whether nimodipine can safely provide similar benefits for people with MS.
The researchers wrote: “These findings underscore the potential of drug repositioning to uncover novel clinical mechanisms for nimodipine and expand its therapeutic applications to other diseases, such as MS.
“Preclinical evidence suggests that nimodipine may attenuate disease severity and demyelination and may promote repair-related processes in rodent models relevant to MS.”
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