Pathophysiology
The brain is made up neurons that are interconnected to form a vase network. These connections known as synapses enable the transmission of information from one neuron to another. In Alzheimer’s disease, ten to fifteen years before the appearance of the symptoms, two main lesions form in the brain, which are senile plaque’s that are composed of Beta-Amyloid protein, and neurofibrillary tangle’s that are composed of Tau protein. On the surface of a neuron is a large protein called APP. Normally, APP is sectioned by enzymes on the surface of the neuron and it frees a protein called Amyloid-Beta. The amyloid-beta protein is then cleared in the body. In the case of Alzheimer’s disease there is an imbalance as the amyloid-beta protein is no longer regulated and is found in two greater quantities. The protein is assembled to form insoluble fibrils and create Senile Plaques. When a neuron communicates with another a signal goes from the body known as soma to the synapse to transfer the information. The signal passes through the skeleton of the neuron composed of microtubules. These microtubules are stabilized by normal towel protein. In Alzheimer’s disease, Tau protein becomes defective and detaches from the microtubules. Thus, the skeleton of the neuron dissociates, as it is no longer maintained. Defective tau protein is then assembled to form filaments in the neuron. Without the skeleton the neurons degenerate and connections between the neurons are lost. The abnormal accumulation of Tau filaments in the neuron creates neurofibrillary tangles and eventually causes the death of the neuron. Neurofibrillary tangles and senile plaques do not follow the same pathway in the brain overtime. Neurofibrillary tangles first develop in the region called the hippocampus, which is essential to memory and learning. They then reach the whole brain following a central