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The symptoms of Alzheimer's disease are a result of changes in the structures of the brain.
A simple analogy helps to explain what happens in the brain when Alzheimer's disease develops. Picture a large city with all its lights on. Each home, street, and shopping center has its own light switch and bulb that lets people go about their daily activities. From an airplane you can see that together these lights make the entire city glow.
Now imagine that a problem occurs with the wiring or circuits within the city's electrical system. Each home, street, and shopping center gradually loses power and the people are unable to carry on as normal. It eventually becomes harder to cook dinner, drive through the city, and do business in stores. The power outage will eventually disable the entire city and its people.
Now think about the brain: imagine that each cell within the brain is a light bulb and the entire brain is the city. Each neuron helps carry out the functions of the brain. During normal function, each neuron and all parts of the brain work together to carry out tasks such as remembering a relative's name, washing the dishes, or controlling one's temper.
Alzheimer's disease gradually "turns off" each neuron in the brain, just like the lights in the city. As the individual neurons stop working, the brain does not function as well and the person has problems thinking, remembering, and carrying on with daily living. However, unlike an electrical circuit that can be repaired, damage in the brain caused by Alzheimer's disease and dementia is permanent and cannot be repaired.
Learn more detailed information about changes that occur in the brain when Alzheimer's disease develops.
Brain Changes with Alzheimer's
The brain changes that happen with Alzheimer's disease take place on both the larger structures and tiny cells in the brain.
The brain is made up of 3 major parts:
- Cerebral cortex (frontal, parietal, occipital and temporal lobes),
- Limbic system (hippocampus, amygdala, thalamus, and more)
- Brain stem (cerebellum, pons, and medulla oblongata)
The Alzheimer's Association provides an interesting, interactive model of the brain here: Inside the Brain
Alzheimer's disease strikes certain parts of the brain first. The limbic system - primarily the hippocampus - is attacked first, then the cerebral cortex, then the brain stem, causing each structure to lose its function in turn. The symptoms that occur are a direct result of this sequential damage:
- Limbic system damage impairs a person's memory and causes mood swings
- Cerebral cortex damage results in trouble controlling emotional outbursts. People at this stage may need help with daily activities, such as eating, shaving or combing hair
- Brain stem damage late in AD impairs organ function, including the function of the heart, lungs, and various other bodily processes.
Normal brain cells (neurons): Neurons are cells in the brain that carry out all brain functions. They have spaces between them called synapses. Brain chemicals, called neurotransmitters, are released by neurons and deposited into the synapses. Neurotransmitters are important for communication between neurons. This communication is responsible for producing movement and is a critical part of learning and remembering. The most common neurotransmitter in the brain is glutamate. Another important neurotransmitter for communication between neurons is acetylcholine.
Alzheimer's effect on brain neurons: At the cellular level, Alzheimer's disease attacks the brain's neurons. Two toxic proteins appear to be responsible for the damage: beta-amyloid and tau. Tangled proteins accumulate within brain neurons. The neurons are eventually destroyed. Scar-like "plaques" accumulate in the brain between the brain's neurons (NIA, 2008).
Beta-amyloid and plaques: In the initial event that leads to AD, part of the neuron that normally helps promote neuron growth and survival breaks down in an abnormal way to produce a toxic protein called beta-amyloid. Beta-amyloid clumps (oligomers) appear to be the most toxic form of the protein. Beta-amyloid damages neurons in at least two ways. It affects the neuron's receptor for a particular neurotransmitter, and that, in turn, interferes with the cell’s ability to function and send messages to other neurons. Beta-amyloid also interferes with another protein that is important for neurons to respond to signals in the hippocampus, a part of the brain that is very important in memory. As the neuron's function is reduced, less of the neurotransmitters are produced and communication between neurons is decreased.
The build-up of "plaques" in the brain, previously thought to be the primary cause of Alzheimer's, now appears to be the result of the damage rather than the primary cause, similar to scar tissue. Composed of protein and fibers surrounding beta-amyloid, plaques may even be an attempt to surround and protect neurons from the toxic effects of beta-amyloid. The rate at which beta-amyloid is made, degraded, or removed from the brain affects the rate at which the plaques are formed. Abnormal "tau" fragments are also found in Alzheimer's plaques.
Tau and tangles (neurofibillary tangles). An abnormal form of another protein called tau also appears to contribute to the development of Alzheimer's disease. Abnormal tau forms tangles of proteins in degenerating neurons. Researchers are currently learning about how this takes place.
Other factors. Changes in the ability to make new blood vessels in the brain or changes in the blood vessels themselves may contribute to a decreased ability to remove beta-amyloid before it causes damage. Changes in the cell cycle of neurons may also contribute to the disease process.
The result of cellular damage: When neurons cannot communicate, learning and memory are impaired. The neurons eventually die. Because of all of this damage, the brain gradually shrinks and becomes less functional, leading to many of the symptoms of dementia.
Knowledge about the cellular level of Alzheimers leads to treatments: Researchers are working to find ways to decrease the amount of beta-amyloid formed or to remove it before it can start damaging the neuron. Similarly, drugs may be developed to block damage from abnormal tau, once it is better understood. Researchers also are trying to find ways to block the progression of neuron damage once it gets started. Many current medications aim to increase the amount of neurotransmitter in the synapse between neurons or to make it more effective at helping a neuron send messages.View References
- Facts About Dementia: Overview
- Alzheimer's Disease: Introduction
- Vascular Dementia: Introduction
- Lewy Body Dementia: Introduction
- Frontotemporal Dementia: Introduction
- Other Types of Dementia
- Diagnosing Dementia
- Treating Dementia