Mitochondria Research Papers

Mitochondria is a double membrane bound organelle in charge of energy production. Mitochondria have their own DNA and manufacture their own ribosomes. They produce mitochondrial DNA and nuclear DNA. Mitochondria can be considered a dynamic organelle because their core function is ATP production. Mitochondria produce about ninety percent of the body’s energy. They migrate within the cells and continuously divide and fuse with each other (Santos, 2010). They are responsible for producing energy to support cell growth. When the mitochondria fail at energy production this results in mitochondrial diseases. These types of mitochondrial diseases are diverse conditions due to malfunctions in the mitochondria or mutations in the mtDNA and nuclear DNA.
Ever since then medical records have shown patients with massive neuronal loss. Alzheimer’s disease is a progressive neurodegenerative disorder. It can be described as a functional disruption of the brain. This disease can take many forms when showing symptoms such as age associated, late onset, familial form, or early onset (Santos, 2010). The progression and onset of this disease is caused by a mitochondrial dysfunction due to degrading cells. Neurons in the brain are the main cells that are destroyed by this disease. Neurons are connections in the brain that communicate at synapses, where then neurotransmitters carry information form one cell to another. Early signs of Alzheimer’s include memory loss that disrupts daily life, difficulty planning and solving problems, confusion with time, problems with speaking words, misplacing items, poor judgment and dramatic changes is mood regularly. Although every individual may not experience all of the symptoms, each symptom can come at any degree. Eighty-three brains obtained at autopsy in 1991 from non-demented and demented individuals were examined for extracellular amyloid deposits and intraneuronal neurofibrillary changes. At the end of the study it was found that end stages of Alzheimer’s are easily recognized at neuropathological exams due to the presence of neurofibrillary changes. (Braak, 1991). The changes result from
It also causes a decrease in white blood cell, called neutropenia. Reoccurring infections often happen because of this. In most cases, Barth syndrome occurs in males, however newly found cases of females being born with this rare condition have been noted. Males mostly get this syndrome because they only have one X chromosome, where the condition is found. In rare cases, some females can have both of their X chromosomes affected. This is often existing at birth. Males who are diagnosed with Barth syndrome at birth often do not usually live long. This syndrome is a severe inherited disorder than can be fatal in childhood. In a study in 1996, it was discovered that Barth syndrome is an X-linked inherited disorder that is that has associated feature of cardiac and skeletal myopathy (Bione, 1996). Also, Barth syndrome has been linked to mutations in the Tafazzin protein, which is found inside of the mitochondria. This protein is made by the TAZ gene. Tafazzin can also be called G4.5. When this gene malfunctions it can cause a misinterpretation between the gene and protein. This protein is made of cardiolipin (Gonzalez, 2005). This lipid is found in the mitochondria’s inner membrane. When the gene malfunctions, the protein is produced with no functional properties. Due to this, Tafazzin cannot modify cardiolipin. This then affects the shape and function of the mitochondria. Barth syndrome has only been