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Molecular Pathology & Alzheimer's Disease - DementiaGuide.com
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Alzheimer's Disease

Molecular Pathology

Alzheimer's disease is characterized by two main landmarks in the brain. They are generally referred to as beta-amyloid plaques and neurofibrillary tangles. Their presence has been linked to the loss of neurons, neuroinflammation and changes in the brain chemicals .

Most cells in the body are enclosed by a membrane made up of proteins and fats. This membrane allows nutrients and waste products to flow in and out of the cell. One of the proteins found in the membrane is called amyloid precursor protein (APP ). Since this protein spans the entire membrane, it is known as a transmembrane protein. Currently, the function of the APP protein is unknown. This protein may be broken down into small pieces that can vary in length. Normally, the protein is cut in a way that does not cause problems. However, in Alzheimer's disease, this protein is cut abnormally. As a result, a toxic , smaller protein called beta-amyloid is produced.

Beta-amyloid is a very sticky protein and has a tendency to clump together. These clumps are known as beta-amyloid plaques. These beta-amyloid plaques are found throughout the outer layer of the brain and the hippocampus . Studies have found that the formation of these plaques is fundamental to the development of Alzheimer's disease. These plaques disrupt communication between neurons, and the cells eventually die.

Neurofibrillary tangles are found inside neurons. It is made up of long proteins that are twisted around each other. They are mostly made up of the protein tau. Tau protein is part of a larger structure that is involved with carrying nutrients to different parts of the neuron. However, in Alzheimer's disease, the tau protein is abnormal. This means that the nutrients cannot be transported properly in the neuron. As a result the neuron becomes damaged and can die.

Molecular Pathology

Source: Holmes, C. (2005). The molecular pathology of Alzheimer's disease. Psychiatry.4 (1) 37-40

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Last updated December 7, 2018
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