Alzheimer disease is a progressive and deadly brain disorder, in which communication between cells are halted and eventually lost. It is the most common form of dementia, and in ~90-95% of AD cases affects those over the age of 65. As communication amongst neurons is lost, symptoms such as inability to recall memories, make appropriate judgment, and proper motor function are lost and worsen over time. Affecting an estimated 2.4 million to 4.5 million Americans, with the number predicted to double within the next few years, preventing the start of Alzheimer is vital.
The brain is divided into three main portions: the cerebrum, the cerebellum, and the brainstem. Though a single organ, each portion is further broken down into sections with distinct control in specific skills. The area most affected by AD is the cerebrum, which is divided into five lobes: frontal, parietal, occipital, temporal, and insula. Each lobe has control over various functions such as memory, voluntary motor functions, different senses, and processing. These actions are conducted through signaling between neurons. These nerve cells contain properties like excitability, conductivity, and secretion. Communication amongst neurons is vital for proper functioning of the whole body.
In a healthy neuron, communication is conducted via neurotransmitters. A presynaptic neuron will release neurotransmitters resulting in the postsynaptic neuron responding to the message. Depending on the location of these nerves in the brain will result in whichever action is taking place. It is the prevention of proper signaling within the brain and cell death that leads to loss of function throughout the body, and ultimately to AD.
Two major contributors to the progression of Alzheimer Disease are the production of beta-amyloid plaques and neurofibrillary tangles. Amyloid Precursor Protein (APP) is believed to assist in neuronal growth and repair. As persistent use is continued, it is potentially broken down and recycled. Alpha-secretase cuts the extracellular portion of APP while gamma-secretase makes its cut in the membrane of the neuron, resulting in a soluble fragment of APP. The creation of beta-amyloid plaque begins when beta-secretase joins alpha-secretase and gamma-secretase in the process of breaking down APP. Beta-secretase creates an addition cut leaving behind an insoluble monomer, amyloid beta. With the characteristic of being sticky, these fragments join together resulting in beta-amyloid plaques. These clumps block signaling at the synaptic cleft, preventing neurotransmission. These plaque buildups trigger an immune response leading to swelling of the brain causing damage to nearby neurons. They also make amyloid angiopathy deposits around blood vessels causing a weakening in the vessel walls. This could lead to hemorrhaging and blood loss.
Neurofibrillary tangles are also extremely prevalent in AD patients, resulting in the degradation of microtubules within the neuron. With the buildup of beta-amyloid plaques, this initiates pathways within the neuron leading to the activation of kinase. Kinase transfers phosphate groups to the tae proteins; this alters the shape of tau protein. A change in shape means a change in function, so tau protein no longer binds the microtubules;
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