%0 Journal Article
%T Mitochondrial therapeutics in Alzheimer's disease and Parkinson's disease
%A Jake G Hoekstra
%A Kathleen S Montine
%A Jing Zhang
%A Thomas J Montine
%J Alzheimer's Research & Therapy
%D 2011
%I BioMed Central
%R 10.1186/alzrt83
%X Mitochondria are organelles serving a wide variety of actions critical to cellular function, several of which are of particular importance to neuronal survival. The primary function of mitochondria is to produce energy in the form of ATP via oxidative phosphorylation, in which electrons are transported down the electron transport chain (ETC) while generating a proton gradient. This gradient drives ATP synthase [1]. Mitochondrial function is particularly important to the central nervous system (CNS) since the CNS uses 20% of the body's resting metabolic energy, 95% of which comes in the form of ATP [1]. Neuronal ATP is essential to the function of the Na+/K+ and Ca2+ ATPases that maintain ion gradients [1,2]. Similarly, mitochondria play a prominent role in Ca2+ buffering by sequestering Ca2+ using ion transporters [1-3]. These actions of mitochondria are especially important to neurotransmission as well as synapse formation and remodeling [3-5]. However, critical roles for mitochondria go beyond ATP production since mitochondria also control cell signaling pathways and cell survival via apoptosis regulation [6]. Mitochondria are now also understood to be dynamic structures that undergo fission and fusion, and the relationships between mitochondrial dynamics and other 'classical' functions are a matter of intense investigation. For these reasons, mitochondria are commonly implicated in neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD).Several neurodegenerative diseases show alterations in mitochondrial DNA (mtDNA) and genes that encode for mitochondria respiratory chain subunits [7]. Similarly, dysfunction of enzymes involved in mitochondrial respiration has been reported in neurodegenerative diseases [7,8]. Such deficits may lead to generation of excessive reactive oxygen species (ROS) and oxidative damage, clearly implicated in several neurodegenerative diseases, or to depletion of ATP [7,8]. Besides damaging tissues direct
%U http://alzres.com/content/3/3/21