Intracellular Nucleocytoplasmic Trafficking in Neurodegenerative Disease

Dear Colleagues,

Survival and growth of eukaryotes is dependent on patterns of gene expression which, in part, are determined by the availability of genes for transcription. The availability of genes for transcription is inherently dependent on the movement of proteins and RNA between the cell nucleus, where the genome is housed, and the cell cytoplasm, where protein synthesis and cellular respiration, among other essential functions, occurs. Conversely, transport between the cell cytoplasm and the nucleus is an essential component of the mechanism that determines how the nucleus, epigenome and DNA structure respond to changes in the cytoplasm. A growing body of evidence has established that mechanisms of exchange between the cell nucleus and cytoplasm, nucleocytoplasmic exchange, are severely disrupted in Alzheimer’s disease, ALS and other neurodegenerative diseases. Yet many aspects of this disruption in nucleocytoplasmic transport remain unknown. What are the upstream mechanisms that initiate altered nucleocytoplasmic transport in neurodegenerative cells and clinical diseases? And what downstream mechanisms couple altered nucleocytoplasmic transport to altered gene expression profiles that result in typical cellular phenotypes of neurodegenerative disease, including synaptic deficits, metabolic disruption, protein processing, etc. What components of the complex nucleocytoplasmic trafficking system are affected in neurodegenerative diseases and where does disruption of normal nucleocytoplasmic exchange fit within the sequential intracellular cellular cascade of neurodegenerative changes? This special issue is designed to provide information that addresses these issues in whole or in part.

Prof. Dr. Paul D. Coleman
Guest Editor

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• nucleocytoplasmic transport
• intracellular trafficking
• neurodegenerative diseases
• Alzheimer’s disease
• Amyotrophic lateral sclerosis
• Frontotemporal dementia
• Huntington’s disease