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Genes and Epigenetic Regulation of Learning and Memory, Addiction, and Parkinson’s Disease


Mitochondrion plays a very vita role in energy transduction in human body especially brain. Mitochondrion has got its own genetic material that helps in coding for polypeptides. It has its complexes I-V that are encoded for by mitochondrion DNA. A review is going to be done on scientific journals that touch on genes and epigenetic regulations of learning and memory, addiction and Parkinson’s disease.

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Gould (2007) asserts that neurogenesis occurs in the brains of adult mammals in the period of their life. This happens in the sub-ventricular zone and the sub-granular zone. Neurons found in the sub-ventricular zone do migrate over long distances to become granule neurons and periglomerular neurons.

Paradies et al 2011 asserts that aging is a biological process that occurs when cells bio-energetic function is impaired and elevated oxidative stress. It can also be occasioned when the cells ability to respond to stress gets attenuated and age related disorders that are related to contracting. This affects tissues of the brain and heart hence an effect on heart and the brain. Oxidative stress is widely believed to contribute to a number of aging processes by rendering the respiratory chain process dysfunctional. When the mitochondrion is exposed to oxidants in the presence of calcium ions, their permeability can be induced. This can have adverse effects on the functions of the mitochondrion. Cardiolipin is pivotal in mitochondrion energy transduction processes. It is also very important in apoptosis. It stabilizes the mitochondrion membrane as well as its dynamics. When the Cardiolipin structure, content, and its hydrocarbon chain profile are changed, the mitochondrion does not function normally in several tissues hence the affected tissues wear out. The electron transport system that takes place in the mitochondria helps a great deal in energy transduction processes in aerobic organisms. This process makes use of five protein complexes that is complex I-V. These are NADH dehydrogenase, succinate dehydrogenase, ubiquinone-cytochrome c oxidoreductase, cytochrome c oxidase, and ATP synthase respectively. Complexes I, III, IV helps in pumping protons across the inner mitochondrial space. This creates an electrochemical gradient used by complex V to generate ATP. Electron transport system helps in generation of ROS. Mitochondrion is therefore the main source of ROS. A significant amount of oxygen that the cell takes up is usually converted by mitochondrion into ROS especially when the mitochondrion produces the superoxide ion. Most of the oxygen that the cells take up are normally used in oxidative phosphorylation. Oxidative phosphorylation however produces a form of a harmful ROS. The effects of the produced harmful ROS are always remedied by an antioxidant defense system (Jiang, 2008). Aging begin to occur when the structures of the protein get modified. Oxidative damage can also substantially contribute to biological aging. The extent to which proteins get damaged by oxidative processes depend heavily on the position of the radical oxidant to the protein that is targeted, the nature of the protein and its location relative to source of the oxidant and the concentration of the available antioxidant. Oxidative damage to proteins makes them loose their ability to perform certain biochemical functions. The proteins that get oxidized because of age related issues may be protein specific rather than being a random process. The brain is quite often affected by damages occasioned oxidation because it has high concentration of peroxidizeable fatty acids. It also has iron that plays part in free radical production. The tissues of the brain are also not sufficient in protective antioxidant enzymes. The regions of brain that get affected by oxidation are the midbrain, hippocampus, and triatum. The regions around the cortex and cerebellum do show very limited evidences of effects of oxidation. The regions of the brain that get affected by the oxidative processes exhibit functional as well as morphological changes with aging. Mitochondrion ROS contribute to aging when they accumulate mutations of mitDNA. Mitochondrial DNA is major target of cellular oxidative damage. When the mitochondrion bioenergetic processes are jeopardized, lethal cell injury can occur. MitDNA is also prone to attack from ROS. The body mitochondrion DNA mutations that occur in one’s life contribute to physiological decline characteristic with aging. These mutations lead to large-scale deletions and point mutations. These activities show that the mitochondrion is experiencing a decline in its functions. Damage of mitDNA is propagated at the time when the cell and the mitochondria divide. This makes the effects of such processes grave. Age related changes to mitochondrion functions could lead to alteration of lipid membrane environment surrounding proteins risk getting altered. Mitochondrial membrane fluidity alterations do affect the respiratory chain activities. Protein gradient also get generated. Phospholipids being the most abundant lipids in the membrane of the cell define membrane permeability barrier as well as modulating the functions of the membrane. The occurrence of polyunsaturated fatty acids in mitochondrial phospholipids renders them the primary target for reactions with oxidizing agents. A number of inner mitochondrion membrane proteins are capable of interacting with Cardiolipin. These membrane proteins comprise the complexes I-V of the electron transport chain. These complexes bind the proteins with a very high affinity (Ballas and Mendel, 2005). The CL plays a very central role in bioenergetic processes. Its ability to interact with proteins helps in formation and stabilization of the super complexes of the mitochondria. Because of the role CL plays in energy transduction process, its alteration in whatever nature can be so deleterious to mitochondrial physiopathology hence changes in mitochondrial bioenergetic parameters like its ability to act as the carrier of anion.

Amo et al., (2011) infer that recessive Parkinson’s disease is necessitated by mutations in PINK1. They allude to the fact that cells that have been cultured get most of their energy from glycolysis. Cells that do not have stable source of energy are able to grow at a very slower rate in normal medium. Cells that grow in galactose medium do oxidize pyruvate through by mitochondrial energy transduction mechanism. Cells that manufacture their energy with the help of mitochondria exhibit growth impairment in media that is enriched with galactose. Growth impairment of human cells in galactose medium is often occasioned by mitochondrial respiratory chain inefficiency. Loss of PINK1 interferes with the functions of the mitochondrion. PINK1 MEF can be a potential PD model hence retarded growth occasioned by decrease in mitochondrion respiratory activity. They are therefore very important in evaluating the roles played by PINK1 and how it influences mitochondrial dysfunction. Fission of mitochondria followed by mitochondrial selective fusion contributes to segregation of mitochondria that has been damaged. These processes contribute decrease in membrane potential hence their autophagy. PINK1-parkin pathway contributes to mitochondrial elimination mechanism. Hence, mitochondrial removal is not required by proton leak but by respiratory chain defects.


Neurosis in mammalian brain occurs in sub-ventricular and sub-granular region. Aging is occasioned by impairment that the bioenergetic processes are subjected to. Oxidative stress is known to render respiratory chain dysfunctional. CL is pivotal in energy transduction process other than being very pivotal in apoptosis.

Reference List

Amo, T. et al., (2011). Mitochondrial membrane potential decrease caused by loss of PINK1 is not due to proton leak, but to respiratory chain defects. Neurobiology of Disease, 41, 111–118.

Ballas, N., and Mandel, G. (2005). The many faces of REST oversee epigenetic programming of neuronal genes. Curr. Opin. Neurobiology. 15, 500–506.

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Gould, E. (2007). How widespread is adult neurogenesis in mammals? Nat. Rev. Neurosci., 8, 481–488.

Jiang, Y. et al., (2008). Epigenetics in the Nervous System. The Journal of Neuroscience. 28(46):11753–11759.

Paradies G. et al., (2011). Mitochondrial dysfunction in brain aging: Role of oxidative stress and Cardiolipin, Neurochemistry International, 58, 447–457.

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StudyCorgi. "Genes and Epigenetic Regulation of Learning and Memory, Addiction, and Parkinson’s Disease." July 22, 2022.


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