Abstract
The atypical antipsychotic agent, clozapine, is used to treat a variety of neurological disorders including schizophrenia and Parkinson’s disease and readily crosses the blood brain barrier to interact with a wide range of neuroreceptors including those for dopamine and serotonin. Recent work has shown that clozapine can reduce neuroinflammation in experimental autoimmune encephalomyelitis, a neuroinflammatory model of multiple sclerosis (MS) and mediates its effects in the central nervous system. To further characterise the protection provided by clozapine, the cuprizone model of demyelination was used to assess the effect of clozapine treatment on the cellular events surrounding demyelination and remyelination. Using this model of non-immune demyelination, we found that clozapine administration was unable to prevent demyelination, but when administered post demyelination, was able to enhance the rate of functional recovery. The more rapid improvement of clozapine-treated mice correlated with a decreased level of astrocyte and microglial activation but only modestly enhanced remyelination. Together, these studies highlight the potential of clozapine to support enhanced functional recovery after demyelination, such as that occurring during MS.
Highlights
Observers were asked to score the level of demyelination (LFB or MBP) based on 3- no visible demyelination, 2= 0-30% demyelination, 1= 30-60% demyelination and 0= 60-90% demyelination
Astrocytes (GFAP) and microglia (Iba-1) were scored on a sliding scale with 3 indicating strong astrocyte activation through to 0 with no visible astrocyte activation
Summary
With images from all different treatment groups mixed together, and given to 3-4 blinded observers.
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