INTRODUCTION
Alzheimer’s disease is a progressive neurodegenerative disorder characterized by memory loss and dementia. The neurodegeneration is due to a formation of amyloid platelets in the brain that interrupt the normal function of it. It worsen with the pass of years and is mostly suffered by older people (Reece et al. 2014).
The platelets composed by Amyloid; a harmful insoluble protein fibril which is produced by Amyloid precursor protein (APP). APP is processed in the membrane of neurons in two different ways called non-amyloidogenic pathway and amyloidgenic pathway. APP production and enzymatic degradation regulate the concentration of Amyloid Beta (Aβ) protein, which is the main component of platelets that cause AD.
The first paper …show more content…
(2010) used AD brain mice models in order to examine the accumulation of synaptic mitochondria, the correlation of mitochondrial Aβ level and aging, and the effect of Aβ on mitochondrial distribution and trafficking along the axons. The methods used in this experiment were the isolation of synaptic and non-synaptic mitochondria of AD mice and non- AD mice at the age of 4 and 12 months. Researchers found out that Aβ levels were higher in AD mice models. Furthermore, the association between the levels of Aβ and the dysfunction of mitochondria were studied by analysing mice at age of 4 months and 12 months. It was concluded that at the age of 12 months the Aβ values were higher than the 4 months mice, showing that with aging the values of Aβ are higher and the risks for AD are greater. The results showed abnormalities on the mitochondria of AD mice models, linking dysfunctional mitochondria with AD. Aβ accumulation and age were linked with increased cyclophilin D (CypD), which was found to be responsible of increased permeability of mitochondrial membrane, leading to imbalance of calcium ions in mitochondria, mitochondrial enlargement and higher reactive oxygen species (ROS) production. In addition, Aβ accumulation was related with oxidative stress in synaptic …show more content…
Another pathway that could allow the entering of Aβ to the mitochondria is CypD which increases the permeability of mitochondrial membrane. Du et al. (2010) showed that CypD levels increases with age, demonstrating that mitochondria get more vulnerable with the pass of time. The accumulation of Aβ inside the mitochondria leads to even more dysfunctionality of the organelle, including calcium disruption, mitochondrial inflammation and oxidative stress (Du et al., 2010). Calcium ions are significantly important in synapsis signalling because enable the release of neurotransmitters to the synaptic cleft and consequently to the postsynaptic cell making the process to continue (Reece et al. 2014). Disruption of calcium ions would cause abnormalities in the synapsis signalling and hence in the function of
Alzheimer’s disease is a progressive neurodegenerative disorder characterized by memory loss and dementia. The neurodegeneration is due to a formation of amyloid platelets in the brain that interrupt the normal function of it. It worsen with the pass of years and is mostly suffered by older people (Reece et al. 2014).
The platelets composed by Amyloid; a harmful insoluble protein fibril which is produced by Amyloid precursor protein (APP). APP is processed in the membrane of neurons in two different ways called non-amyloidogenic pathway and amyloidgenic pathway. APP production and enzymatic degradation regulate the concentration of Amyloid Beta (Aβ) protein, which is the main component of platelets that cause AD.
The first paper …show more content…
(2010) used AD brain mice models in order to examine the accumulation of synaptic mitochondria, the correlation of mitochondrial Aβ level and aging, and the effect of Aβ on mitochondrial distribution and trafficking along the axons. The methods used in this experiment were the isolation of synaptic and non-synaptic mitochondria of AD mice and non- AD mice at the age of 4 and 12 months. Researchers found out that Aβ levels were higher in AD mice models. Furthermore, the association between the levels of Aβ and the dysfunction of mitochondria were studied by analysing mice at age of 4 months and 12 months. It was concluded that at the age of 12 months the Aβ values were higher than the 4 months mice, showing that with aging the values of Aβ are higher and the risks for AD are greater. The results showed abnormalities on the mitochondria of AD mice models, linking dysfunctional mitochondria with AD. Aβ accumulation and age were linked with increased cyclophilin D (CypD), which was found to be responsible of increased permeability of mitochondrial membrane, leading to imbalance of calcium ions in mitochondria, mitochondrial enlargement and higher reactive oxygen species (ROS) production. In addition, Aβ accumulation was related with oxidative stress in synaptic …show more content…
Another pathway that could allow the entering of Aβ to the mitochondria is CypD which increases the permeability of mitochondrial membrane. Du et al. (2010) showed that CypD levels increases with age, demonstrating that mitochondria get more vulnerable with the pass of time. The accumulation of Aβ inside the mitochondria leads to even more dysfunctionality of the organelle, including calcium disruption, mitochondrial inflammation and oxidative stress (Du et al., 2010). Calcium ions are significantly important in synapsis signalling because enable the release of neurotransmitters to the synaptic cleft and consequently to the postsynaptic cell making the process to continue (Reece et al. 2014). Disruption of calcium ions would cause abnormalities in the synapsis signalling and hence in the function of