Alzheimer's disease-audio

Alzheimer’s disease is a progressive degenerative disorder of the cerebral cortex, especially the frontal lobe. It affects approximately 4 million Americans; by 2040, that figure may exceed 6 million.
The disease has a poor prognosis. Typically, the duration of illness is 8 years, and patients die 2 to 5 years after onset of debilitating brain symptoms.
Causes
Exact cause unknown
Possible contributing factors
Genetic patterns
Beta-amyloid plaque development
Inflammatory and oxidative stress processes
The role of estrogen in the brain
Pathophysiology
The brain of a patient with Alzheimer’s disease has three characteristic features: neurofibrillary tangles (fibrous proteins), neuritic plaques (composed of degenerating axons and dendrites), and neuronal loss (degeneration).
Neurofibrillary tangles are bundles of filaments found inside neurons that abnormally twist around one another. Abnormally phosphorylated tau proteins accumulate in the neurons as the characteristic tangles and ultimately cause neuronal death. In a healthy brain, tau provides structural support for neurons, but in patients with Alzheimer’s disease this structural support collapses.
Neuritic plaques (senile plaques) form outside the neurons in the adjacent brain tissue. Plaques contain a core of beta-amyloid protein surrounded by abnormal nerve endings or neurites. Overproduction or decreased metabolism of beta-amyloid peptide leads to a toxic state causing degeneration of neuronal processes, neuritic plaque formation, and eventually neuronal loss and clinical dementia.
Tangles and plaques cause neurons in the brain of the patient with Alzheimer’s disease to shrink and eventually die, first in the memory and language centers and finally throughout the entire brain. This widespread neuron degeneration leaves gaps in the brain’s messaging network that may interfere with communication between cells, causing some of the symptoms of Alzheimer’s disease.
Signs and symptoms
Mild
Disorientation to date
Impaired recall
Diminished insight
Irritability
Apathy
Moderate
Increased disorientation (time and place)
Fluent aphasia
Difficulties with comprehension
Impaired recognition
Poor judgment
Trouble performing activities of daily living (ADLs)
Aggression
Restlessness
Psychosis
Sleep disturbances
Dysphoria
Severe
Unable to use language appropriately
Memory only to the moment
Needs assistance with all ADLs
Urinary and fecal incontinence
Diagnostic test results
Neuropsychologic evaluation shows deficits in memory, reasoning, vision-motor coordination, and language function.
Magnetic resonance imaging or computed tomography scan reveals brain atrophy at later stages of the disease.
Positron emission tomography scanning shows decreased brain activity.
EEG shows evidence of slowed brain waves at later stages of the disease.
Treatment
Cholinesterase inhibitors, such as tacrine, donepezil, rivastigmine, and galantamine
Behavioral therapy
Nonsteroidal anti-inflammatory drugs
Cholesterol-lowering drugs
Estrogen

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