Dear Colleagues,

In the last year, neurodegeneration has become an increasing focus of neuroscience research. Neurodegenerative disorders, featuring the progressive dysfunction and death of cells in selected areas of the nervous system, are associated with conformational changes in proteins that result in the extra- and intracellular accumulation of misfolded proteins like alpha-synuclein, tau, TDP-43 and others, representing the hallmarks of many neurodegenerative diseases, summarized as proteinopathies. Strains of pathological proteins propagate in a protein-like manner across the nervous system, thus promoting the neurodegenerative process. Major basic mechanisms caused by genetic, environmental and endogenous factors are oxidative stress, proteasomal deficiency, mitochondrial dysfunction, impaired bioenergetics and neuroinflammation, which, in complex interrelation, lead to neuronal death, synaptic dysfunction and the disruption of axonal transport. The glial contribution to neurodegeneration was largely underestimated until recently. Accumulating experimental evidence has suggested that astroglia and oligodendroglia, affected by aberrant cytoplasmic aggregations, act as important mediators of neurodegeneration, while astrocytes represent an essential link between degeneration, regeneration and neuroprotection. The activation of microglia induced by pro-inflammatory agents and cytokine involvement plays an important role in neuroinflammation and contributes to the progression of neurodegeneration. Further important goals of modern neuroscience are the elucidation of stress signaling in the post-translational processing of neuronal death. Chloroplast and dysregulated mitochondrial bioenergetics are important factors in the pathophysiology of neurodegeneration. Growing evidence reveals the importance of ion channels, which play a crucial role in cell homogenesis, signal transduction and neurotransmitter secretion. The elucidation of these basic cellular mechanisms associated with gene expression will provide better insight into the complex pathomechanisms of neurodegenerative disorders as a possible basis for further development of disease-modifying treatment options for these detrimental disorders.

Prof. Dr. Kurt A. Jellinger
Guest Editor

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