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Amyloid Beta Peptide

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Magnetic Resonance Imaging (MRI) is used to show the borders of white and gray matter in the brain. This can help to differentiate AD from multi infarct dementia and low pressure hydrocephalus based on the ratios of white and gray matter. A person with AD suffers from a loss of gray matter, thus making the ratio of gray to white matter smaller than in a person without AD. An exam of the body fluid and non-neural tissue can be helpful to differentiate between AD and other disorders and infections that cause changes in the blood and CSF. These tests also help to demonstrate the functionality of neurotransmitters, metabolites, and enzymes. Although these tests are useful, the only way to confirm that a patient definitely has AD is by autopsy…show more content…
This specific gene codes for amyloid beta peptides. The amyloid beta peptides are found in the plaques associated with AD and also in the neurofibrillary tangles. Accumulation of this peptide may cause AD. There is usually too much accumulation of amyloid beta in the brain and not enough clearance. The build up then causes the plaques and tangles. It is believed that a missense mutation in the precursor for this peptide is what causes an imbalance between accumulation and clearance. Also, when the amyloid beta forms deposits in the neurons, it is believed to stimulate activity of microglial cells. When these cells are stimulated, it causes the production of more amyloid beta, accounting for the progression of the disease. This theory is known as the amyloid beta cascade hypothesis. Although there are many supporters of this theory, there still is not enough evidence to prove it and there is some evidence against it. Firstly, there is not a mutation in the amyloid gene that increases the risk of familial AD. Amyloid beta has also been shown to be non toxic, so it alone can not account for the death of neurons in the brain associated with AD. However, the stimulation of the microglial cells also results in the production of tau proteins, which when in excess, may be the cause of neuronal death. Also, the microglial activation might cause the release of other neurotoxic molecules, such as IL-1b, IL-6, TNFa, nitric oxide, and many other
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