Mitochondria in Neuroplasticity and Neurological Disorders

Mitochondria in Neuroplasticity and Neurological Disorders

December 11, 2008 | Mark P. Mattson, Marc Gleichmann, Aiwu Cheng
The chapter discusses the critical role of mitochondria in neuroplasticity and neurological disorders. Mitochondria are essential for generating ATP, regulating Ca2+ and redox signaling, and mediating synaptic plasticity. They are highly dynamic organelles that undergo fission and fusion, and their transport within neurons is crucial for maintaining metabolic demand in different regions. Mitochondrial dysfunction can lead to neuronal death through necrosis or programmed cell death (PCD), such as apoptosis. In ischemic stroke, mitochondria play a key role in neuronal death by generating reactive oxygen species (ROS), accumulating Ca2+, and forming permeability transition pores (PTPs). In Alzheimer's disease, mitochondrial dysfunction is linked to amyloid β-peptide (Aβ) accumulation, oxidative stress, and impaired Ca2+ homeostasis. The chapter also highlights the importance of mitochondrial dynamics, such as fission and fusion, in maintaining neuronal health and plasticity. Advances in understanding mitochondrial biology are leading to novel approaches for preventing and treating neurological disorders.The chapter discusses the critical role of mitochondria in neuroplasticity and neurological disorders. Mitochondria are essential for generating ATP, regulating Ca2+ and redox signaling, and mediating synaptic plasticity. They are highly dynamic organelles that undergo fission and fusion, and their transport within neurons is crucial for maintaining metabolic demand in different regions. Mitochondrial dysfunction can lead to neuronal death through necrosis or programmed cell death (PCD), such as apoptosis. In ischemic stroke, mitochondria play a key role in neuronal death by generating reactive oxygen species (ROS), accumulating Ca2+, and forming permeability transition pores (PTPs). In Alzheimer's disease, mitochondrial dysfunction is linked to amyloid β-peptide (Aβ) accumulation, oxidative stress, and impaired Ca2+ homeostasis. The chapter also highlights the importance of mitochondrial dynamics, such as fission and fusion, in maintaining neuronal health and plasticity. Advances in understanding mitochondrial biology are leading to novel approaches for preventing and treating neurological disorders.
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[slides and audio] Mitochondria in Neuroplasticity and Neurological Disorders