Exocytosis, Mitochondrial Injury and Oxidative Stress in Neurodegenerative Diseases

Abstract

AbstractCommon features seen in the early stages of many neurodegenerative diseases include increases in oxidative stress and mitochondrial dysfunction, ultimately leading to defects in cellular energy production. These changes particularly affect cells that are highly active, such as neurons. As such, reduced synaptic transmission is a common early feature associated with neurodegenerative diseases, such as Parkinson s disease, Alzheimer s disease, Huntington s disease and Amyotrophic Lateral Sclerosis. Many genes associated with neurodegenerative diseases are now known to regulate either mitochondrial function, redox state or the exocytosis of neurotransmitters. Mitochondria are a significant source of cellular ATP and reactive oxygen species and are prevalent in synapses at areas of exocytosis. Therefore, it follows that reductions in mitochondrial function and/or increases in oxidative stress will impact on neurotransmission.KeywordsMitochondriaOxidative stressExocytosisNeurotransmissionSynaptic transmissionSNARE proteinsLong-term potentiationβ-amyloidAlzheimer s diseaseParkinson s diseaseAmyotrophic lateral sclerosisHuntington s disease