Neurodegenerative diseases are a major clinical and social problem in our times, hence an intensive search for neuroprotective drugs seems fully justified. Recent decades have witnessed fast development of the biochemical theories of neuronal death and survival and in consequence new approaches to the treatment of neurodegenerative diseases based on a cell and a gene therapy have been proposed. The classic excitotoxic cascade theory still remains valid, but has been enriched with new findings on the mechanism of apoptosis. Besides, a stronger emphasis has been put on the role of mitochondria in neuronal damage. Apart from agents that interfere with particular phases of excitotoxic cascades such as, e.g., pathological activation of ionotropic and metabotropic glutamatergic receptors, activation of voltage-dependent calcium and sodium channels, free radicals formation and activation of neuronal nitric oxide synthase, some new potential neuroprotective drugs have been recently suggested, e.g. neuropeptides, endocanabinoids, protein kinase inhibitors, erythropoietin, prostanoid receptor agonists, targeted neurotrophins and some immunosuppressants. However, despite indisputable progress in molecular and genetic sciences, no neuroprotective drug has been designed so far. There are at least two main reasons for this failure. First, our knowledge of the mechanism of neuronal death and survival is still incomplete. Genomic and proteomic analyses provide us with a plethora of new data, but there are still serious problems with their correct and straightforward interpretation. Moreover, better animal transgenic models of neurodegenerative diseases are required, and in vitro models should be based on human rather than animal neuronal cell lines, since the composition of protein targets for new drugs may show remarkable species differences. Second, there are no clear indications how these drugs should be used in the clinic. A number of putative neuroprotective drugs possess a narrow time-window, have dual activity (pro- or antiapoptotic, depending on the concentration, the type of a neuronal tissue and the stage of its development), or unfavourable pharmacokinetic parameters. Therefore it seems that further improvement of the outcome of neurodegenerative disease treatments may depend not only on a better understanding of the molecular mechanism of neuronal pathology and survival, but also on the beneficial biopharmaceutical properties of neuroprotective agents and on well-designed clinical trials.

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1. Emulsion-core and (bio)polyelectrolyte shell nanocapsules for neuroprotective drug delivery