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Effects of behaviorally active ACTH (4-10) analogue - Semax on rat basal forebrain cholinergic neurons
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
In this rat cell study, the authors examined Semax (Met-Glu-His-Phe-Pro-Gly-Pro), an ACTH(4-10) analogue, on cholinergic basal forebrain neurons in vitro. Primary neuronal and glial cultures from rat basal forebrain were used. Semax stability in culture was tested by HPLC, and cell survival was assessed by immunocytochemical and cytochemical analyses and choline acetyltransferase activity. The abstract reports that Semax approximately 1.5-1.7-fold increased survival of cholinergic basal forebrain neurons in vitro, and that Semax (100 nM) stimulated choline acetyltransferase activity in dissociated basal forebrain cultures. The numbers of GABA-ergic neurons and total neuron-specific enolase neurons were not affected. From 1 nM to 10 microM, Semax did not affect glial cell proliferation. The authors state that implications for Alzheimer's disease remain to be clarified.
Abstract
It is well established that cholinergic neurons of the basal forebrain degenerate in Alzheimer's dementia. Although recent studies were concentrated on screening molecules that might reduce the concomitant cell loss, little is known about therapeutically promising molecules. We studied the effect of Semax (Met-Glu-His-Phe-Pro-Gly-Pro), a behaviorally active adrenocorticotropic hormone (4-10) analogue, on survival of cholinergic basal forebrain neurons in vitro. Semax is known to stimulate learning and memory and can be successfully used for treatment of ischemic stroke. Primary cultures of neuronal and glial cells from basal forebrain of rats were used in all experiments. The stability of Semax in cell cultures was tested by HPLC analysis. Cell survival in neuronal cultures was quantitated using immocytochemical and cytochemical analyses as well as detection of choline acetyltransferase activity. We have shown that Semax may approximately 1.5-1.7 fold increase survival of cholinergic basal forebrain neurons in vitro. Moreover, Semax (100 nM) stimulated activity of choline acetyltransferase in dissociated basal forebrain tissue cultures. However, the numbers of GABA-ergic neurons, total neuron specific enolase neurons were not affected. In concentration from 1 nM to 10 microM, Semax did not affect proliferation of glial cells in primary cultures. Implications of these findings with respect to Alzheimer's disease remain to be clarified.
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