Since cytoskeletal alterations are among the most common neuropathological features observed in a variety of neurodegenerative disorders, in the first paper we investigated the relationship between cytoskeletal changes induced by colchicine and the onset of neuronal apoptosis. In fact, taxol stabilises microtubules and prevents nuclear fragmentation.
Cytoskeletal alterations are also present in neuronal damage elicited by excitatory amino acids.
Therefore, we explored the possibility that cytoskeletal elements could be involved in NO-induced apoptosis. Besides nitric oxide's physiological functions, it has been shown that NO can mediate, at least in part, glutamate toxicity through the formation of peroxynitrite. NO or its products induces either apoptotic or necrotic cell death depending on the intensity of the insult. An early dissolution of actin filaments, followed by a breakdown of microtubules and nuclear lamins, precedes the appearance of typical apoptotic features. In parallel, in the fourth paper we investigated the potential toxicity of glutamate in CGCs.