Alzheimer's Disease Lab Report

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Mitochondrial dysfunction: Alzheimer’s disease

In the second Lab assignment, we had the opportunity to study and analyze de cell structure and its functions. Taking that as a reference, we all know that there is no way to talk about life without talking about energy in the human body. These two words are related to each other. Energy in the human body is adenosine triphosphate (ATP), and ATP is the “fuel” that keep the cells in our multicellular body working (metabolism). Mitochondria primary role is to produce ATP. In other words, mitochondria are the power plants that produce the energy that your body utilize to keep you moving around (jumping, jogging, and breathing). Mitochondria contain their own DNA and RNAs (tRNAs and rRNAs) (Devlin, …show more content…
al., 2010). AD symptomatology is characterized by memory loss (Moreira, et. al., 2010). In most of the cases of Alzheimer’s disease, there is a relationship between inheritance and gene susceptibility (Moreira, et. al., 2010). AD familial cases are caused by mutations in the gene related to the amyloid beta precursor protein (ABPP) presenilin one and two (PS1 & PS2) (Moreira, at. al., 2010). There are two incredibly important hallmarks that you can find when you autopsy a brain with AD: in the extracellular area, you will find extracellular senile plaques (SP) in the neocortex and the hippocampus. Also, in the intracellular area, you will find the intracellular neurofibrillary tangles (NFTs) (Moreira, et. al., …show more content…
al., 2010). Furthermore, some studies show significant changes in the mitochondria before the first symptoms of the disease (Moreira, et. al., 2010). Moreover, it has been demonstrating that mitochondrial dysfunction and oxidative abnormalities occur before the formation of amyloid beta plaques (AB) (Moreira, at. al., 2010). Moreover, the accumulation by overproduction of AB can cause a significant imbalance in the mitochondrial dynamics causing mitochondrial fragmentation and abnormality distribution of mitochondria inside neurons (Arrázola, et. al., 2015). Furthermore, there are evidences that suggested that persistent activation of Wnt signaling molecules through Wnt ligands, or inhibition of negative signalers such as glycogen synthase kinase-3B (GSK-3B) and Dickkopf-1 (DKK-1), which can be found high in patients with AD, can be a good approach against the high toxicity of AB and ameliorate cognitive presentation in AD (Wan, et. al.,
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