Sj. Harper et al., CEP-1347 increases ChAT activity in culture and promotes cholinergic neurone survival following fimbria-fornix lesion, NEUROREPORT, 11(10), 2000, pp. 2271-2276
Recent evidence suggests that the activation of the Jun N-terminal kinase (
JNK) signal transduction pathway may be important in neuronal responses to
stresses such as trophic factor deprivation. Preventing the activation of J
NK and expression of c-Jun may, therefore, be neuroprotective. Here, we rep
ort that the small molecule CEP-1347, which has been shown to inhibit the J
NK signalling pathway, promotes cholinergic activity in cultured embryonic
septal neurones. In vivo, we have shown that CEP-1347, administered either
by sub-cutaneous. (s.c.) injection or by continuous infusion, is partially
neuroprotective, for cholinergic neurones in the medial septum, following f
imbria-fornix transection. These data suggest that small molecules such as
CEP-1347 may have beneficial effects in treating neurodegenerative diseases
. NeuroReport 11:2271-2276 (C) 2000 Lippincott Williams & Wilkins.