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Senile dementia and Alzheimer's disease are progressive, degenerative, neurological disorders that result in memory impairment and deterioration in cognitive function, reasoning, and behavior of the individual. Alzheimer's disease is the most common form of dementia - accounting for more than 60 percent of late life disorders of cognitive dysfunction. The loss of intellectual function initially interferes with daily life, and after a disease course that may last many years, eventually results in death. Death is usually due to factors such as compromised nutrition, complications of the immune system (pneumonia, sepsis, other infections), trauma, or aspiration.(1)
Neuronal destruction that manifests as cortical atrophy, degeneration of the cholinergic neurons, accumulation of neuritic plaques and neurofibrillary tangles are observed in the brains of individuals afflicted with Alzheimer's disease. A specific protein, beta amyloid, is found at the center of neuritic plaques. Other factors that may mediate the progression of the disease include concentrations of apolipoprotein E, inflammatory mediators such as prostaglandins, and the degree of cholinergic neuronal activity.
For decades, scientists have been trying to determine which of the brain lesions associated with Alzheimer's disease is more important, the plaques that increasingly develop in the spaces between nerve cells, or the neurofibrillary tangles that develop inside the nerve cells. Scientists are still trying to determine which of these abnormalities occurs first, or whether they occur simultaneously, and what is it that triggers their development in the brains of patients with Alzheimer's disease.
Beta amyloid is a protein that is produced from enzymes called secretases, which occur on the surface of brain cells. One of the leading theories in Alzheimer's disease is related to the fact that the cells in the brains of people with AD produce way too much beta amyloid, especially an unusually "sticky" variant of the protein. It is the excess production of beta amyloid protein that apparently forms the characteristic plaque deposits that accumulate, especially in the hippocampus and amygdala sections of the brains of AD patients. When these beta amyloid plaque deposits grow larger, they trigger an inflammatory reaction in the brain's immune system that begins to kill surrounding brain cells.(2) Researchers are now developing a class of drugs called secretase inhibitors that may be able to inhibit the excess production of beta amyloid to use in the prevention and treatment of Alzheimer's disease.(3)
APOE: In 1992 a gene that increases the risk to Alzheimer's disease was discovered. APOE is a lipoprotein that plays a key role in the metabolism of cholesterol. A variant of this gene, known as APOE4, is a known risk factor for heart disease. Researchers are now wondering if people with the APOE4 version of this gene are also at greater risk of developing Alzheimer's disease.(4)
Tau is a protein that functions as structural support for the vast network of microtubules that exist throughout the brain. Chemical changes cause tau molecules to change shape, which results in a distortion of the microtubules. As the microtubules begin to twist and tangle, the surrounding cells begin to shrink and die. In addition to being a theory about Alzheimer's disease, it is being suggested that measuring levels of specific tau proteins in the cerebral spinal fluid may be useful in the diagnosis of Alzheimer's disease.(5)
Cholinergic neurons in the cerebral cortex are the primary site of cellular degeneration in Alzheimer's disease, causing a decline in the production of the neurotransmitter acetylcholine, which regulates many memory-related functions.(6) There is also evidence that other neurotransmitters such as serotonin,<
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