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Genetic factors: Genetic factors are known to play a role in some cases of Alzheimer's disease (AD). A gene, called the amyloid beta precursor protein (APP) gene, has been linked to the occurrence of AD in Down's syndrome patients who survive beyond 40 years. Some families with a history of early-onset AD also have a mutation on the APP gene. Another gene, the Apo E gene, also has been implicated in the disease. Apo E is a protein found with beta amyloid (a protein found in the brains of AD patients) in neuritic (inflamed nerve) plaques. Together, these genetic mutations account for less than 10% of all AD cases. Plaques and tangles: The causes of Alzheimer's disease (AD) are poorly understood, but its effect on brain tissue has been demonstrated clearly. AD damages and kills brain cells. A healthy brain has billions of nerve cells called neurons. Neurons generate electrical and chemical signals that are relayed from neuron to neuron to help an individual think, remember, and feel (physically and emotionally). Brain chemicals called neurotransmitters help these signals flow seamlessly between neurons. Initially in people with AD, neurons in certain locations of the brain begin to die. When they die, lower levels of neurotransmitters are produced, creating signaling problems in the brain. One neurotransmitter, known as acetylcholine, has been found to be deficient in the brains of those with AD. Medication treatment is based around increasing the amount of acetylcholine in the brain.
Plaques and tangles in brain tissue are considered hallmarks of Alzheimer's disease. Studies of plaques and tangles from the brains of people who have died of AD suggest several possible roles these structures might play in the disease.
Plaques are made up of beta-amyloid, a normally harmless protein. Although the ultimate cause of neuron death in AD is not known, mounting evidence suggests that a form of beta-amyloid protein may be the cause. The plaque is responsible for memory deterioration in individuals with AD.
The internal support structure for brain neurons depends on the normal functioning of a protein called tau. In people with AD, threads of tau protein undergo alterations that cause them to become twisted or tangled. Many researchers believe that this may seriously damage neurons, causing them to die. Inflammation: Researchers have observed inflammation in the brains of some people with AD. Inflammation is the body's response to injury or infection and a natural part of the healing process. Even as beta-amyloid plaques develop in the spaces between neurons, immune cells are at work getting rid of dead cells and other waste products in the brain. Although research has found that the inflammation occurs before plaques have fully formed, it is not known how this development relates to the disease process. There is also debate about whether inflammation has a damaging effect on neurons or whether it is beneficial in clearing away plaques.
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