The CNTF-derived peptide mimetic Cintrofin attenuates spatial-learning deficits in a rat post-status epilepticus model

- We report first in vivo efficacy data for the novel CNTF peptide mimetic Cintrofin.
- Impact of Cintrofin was evaluated in a rat post-status epilepticus model.
- Cintrofin prevented long-term alterations in number of neuronal progenitor cells.
- Cintrofin significantly attenuated the persistence of basal dendrites.
- Cintrofin exerted beneficial effects on disease-associated cognitive impairment.

Ciliary neurotrophic growth factor is considered a potential therapeutic agent for central nervous system diseases. We report first in vivo data of the ciliary neurotrophic growth factor peptide mimetic Cintrofin in a rat post-status epilepticus model. Cintrofin prevented long-term alterations in the number of doublecortin-positive neuronal progenitor cells and attenuated the persistence of basal dendrites. In contrast, Cintrofin did neither affect acute status epilepticus-associated alterations in hippocampal cell proliferation and neurogenesis nor reveal any relevant effect on seizure activity. Whereas status epilepticus caused a significant disturbance in spatial learning in reversed peptide-treated rats, the performance of Cintrofin-treated rats did not differ from controls. The study confirms that Cintrofin comprises an active sequence mimicking effects of its parent molecule. While the data argue against an antiepileptogenic effect, they indicate a putative disease-modifying impact of Cintrofin.