Alzheimer’s disease is the most common dementia in elderly presented in more than 5 million Americans. It is an irreversible and progressive brain disease that accounts for 60-80% of cases of dementia in the elderly. The symptoms can appear after the age of 60-65 to population over 85 years old. This disease slowly destroys memory and thinking skills, followed by failure of language skills, visual-spaced orientation, judgment and eventually even the ability to carry out the simplest tasks in a person’s daily life and activities. [1] There are three know causes for this disease. Production of plaques, collection of intraneuronal cytoskeletal filaments called neurofibrillary tangles produced and the loss of connections between nerve cells responsible for learning and memory. [2] This paper will discuss the first two causes, and the difference between the normal pathways and abnormalities on them present on Alzheimer’s disease.
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Alois Alzheimer examined a female’s brain who had died from a mental illness. In her autopsy he discovered many abnormal plaques and tangle bundle of fibers around the nerve cells. The plaques now a day are known as Amyloid plaques, which are made up of fragments of a protein called beta-amyloid peptide (Aβ) mixed with a collection of additional proteins, remnants of neurons, and bits and pieces of other nerve cells. To describe where Aβ originates, first we have to talk about the APP gene.
APP gene is located on chromosome 21 and tells the cells how to make amyloid precursor protein. His protein is found in many tissues and organs, including CNS. Amyloid precursor protein is cut by enzymes to create peptides. There are two pathways that APP execute:
- Non-plaque formation: in this process APP is cleaved in two important components for the cell a N terminal sAPPa, involved on neuronal outgrowth and survival, and a C-terminal, CTFa involved on nuclear
Alois Alzheimer examined a female’s brain who had died from a mental illness. In her autopsy he discovered many abnormal plaques and tangle bundle of fibers around the nerve cells. The plaques now a day are known as Amyloid plaques, which are made up of fragments of a protein called beta-amyloid peptide (Aβ) mixed with a collection of additional proteins, remnants of neurons, and bits and pieces of other nerve cells. To describe where Aβ originates, first we have to talk about the APP gene.
APP gene is located on chromosome 21 and tells the cells how to make amyloid precursor protein. His protein is found in many tissues and organs, including CNS. Amyloid precursor protein is cut by enzymes to create peptides. There are two pathways that APP execute:
- Non-plaque formation: in this process APP is cleaved in two important components for the cell a N terminal sAPPa, involved on neuronal outgrowth and survival, and a C-terminal, CTFa involved on nuclear