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Alzheimer’s disease
Prior theories regarding the accumulation of aluminum, lead, mercury, and other substances in the brain leading to AD have been disproved. The only way to know for certain that someone had AD is by microscopic examination of a sample of brain tissue after death. The brain tissue shows "neurofibrillary tangles" (twisted fragments of protein within nerve cells that clog up the cell), "neuritic plaques" (abnormal clusters of dead and dying nerve cells, other brain cells, and protein), and "senile plaques" (areas where products of dying nerve cells have accumulated around protein). Although these changes occur to some extent in all brains with age, there are many more of them in the brains of people with AD. The destruction of nerve cells (neurons) leads to a decrease in neurotransmitters (substances secreted by a neuron to send a message to another neuron). The correct balance of neurotransmitters is critical to the brain. Text Continues Below
By causing both structural and chemical problems in the brain, AD appears to disconnect areas of the brain that normally work together. About 10 percent of all people over 70 have significant memory problems and about half of those are due to AD. The number of people with AD doubles each decade past age 70. Having a close blood relative who developed AD increases your risk. Early onset disease can run in families and involves autosomal dominant, inherited mutations that may be the cause of the disease. So far, three early onset genes have been identified. Late onset AD, the most common form of the disease, develops in people 60 and older and is thought to be less likely to occur in families. Late onset AD may run in some families, but the role of genes is less direct and definitive. These genes may not cause the problem itself, but simply increase the likelihood of formation of plaques and tangles or other AD-related pathologies in the brain.
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