2.1.4 Memory and Oxidative Stress
Oxidative stress has an important role in the generation of many human diseases (Rajendran et al., 2014). Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are produced continuously in the body via oxidative metabolism, mitochondrial bioenergetics, and immune function (Roleira et al., 2015). The most common types of ROS include superoxide anion, hyphochlorous acid, hydrogen peroxide, singlet oxygen, hypochlorite, hydroxyl radical, and lipid peroxides, which have a vital role in cell progression, growth, death, and differentiation. They can join with nucleic acids, enzymes, membrane lipids, proteins, and other small molecules (Rajendran et al., 2014). Nuclear factor-kappa B (NF-?B) manage the inflammation resulted from the short-term postprandial mitochondrial oxidative stress (Jung et al., 2009).
Normally, the production of ROS is managed by multiple antioxidant systems (Gandhi and Abramov, 2012). Oxidative stress is a status of imbalance between ROS generation and antioxidant protection, resulting in huge overgrowth of ROS (Ray et al., 2012). Oxidative stress has many different mechanisms includes cell membrane damage from lipid peroxidation, alterations in protein structure and role as aresult of protein oxidation, and structural damage to DNA (Gandhi and Abramov, 2012).
The most metabolically active organs in the body is the brain, it is affected by oxidative stress mainly because of the following causes. Firs, high oxygen demand of the brain, that may reach 20% of the body oxygen use. Second, the presence of high number of redox-active metals such as iron or copper and they catalyze ROS production. Third, the brain cell membranes polyunsaturated fatty acids are highly reactive and represent a substrates for lipid peroxidation(Wang and Michaelis, 2010). Finally, GSH in the brain levels in the brain is low, that have an impact of endogenous antioxidant in the removal of ROS (Ferreira et al., 2015).
Oxidative imbalance and the resulted neuronal damage may be an essential cause in the begining and development of AD (Wang et al., 2014). Memory and learning malfunctions are stimulated by injecting of A?1-42 into the mice bilateral hippocampus and were suppressed by diverse antioxidants (Li et al., 2014, Yu et al., 2015, Chu et al., 2012).
2.1.5 Memory and BDNF
The neurotrophin BDNF (brain-derived neurotrophic factor) is an individual from a group of neurotrophic factors basically engaged with directing the survival and separation of neuronal populaces amid advancement (Huang and Reichardt, 2001). An incredible group of confirmation shows additionally that BDNF directs the structure and elements of various neuronal circuits all through life (Lu et al., 2009).
Steady with the view that action subordinate changes in synaptic quality underlie memory handling and capacity (Kandel, 2001), a developing assortment of confirmation rose proposing that BDNF assumes a urgent part in learning and memory (Lu et al., 2009).
Numerous hippocampus and additionally amygdala-subordinate learning assignments, including dread elimination, are joined by particular changes in BDNF mRNA and protein handling, requiring ideal levels of endogenous BDNF to shape stable recollections. For instance, acknowledgment memory builds BDNF discharge and actuates ERK2 in the dentate gyrus and the perirhinal cortex(K. and M., 2012).
BDNF is associated with the development of various sorts of recollections and is likewise basic for keeping up dependable capacity of data in hippocampus, amygdala and separate cortex numerous hours subsequent to learning happens. BDNF might be important to check the regular procedure of memory rot, which is run of the mill in maturing and is exacerbated in some neurodegenerative disorders(K. and M., 2012).
2.1.4 Memory and Oxidative Stress