Alzheimer and Parkinson Diseases

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Alzheimer and Parkinson diseases are degenerative disorders of the brain associated with neurotransmitter deficiencies.

Alzheimer29disease (AD) may begin before the age of 50 with symptoms so slight and ambiguous that early diagnosis is difficult. One of its first symptoms is memory loss, especially for recent events. A person with AD may ask the same questions repeatedly, show a reduced attention span, and become disoriented and lost in previously familiar places. Family members often feel helpless and confused as they watch their loved one's personality gradually deteriorate beyond recognition. The AD patient may become moody, confused, paranoid, combative, or hallucinatory—he or she may ask irrational questions such as, Why is the room full of snakes? The patient may eventually lose even the ability to read, write, talk, walk, and eat. Death ensues from pneumonia or other complications of confinement and immobility.

AD affects about 11% of the U.S. population over the age of 65; the incidence rises to 47% by age 85. It accounts for nearly half of all nursing home admissions and is a leading cause of death among the elderly. AD claims about 100,000 lives per year in the United States.

Diagnosis of AD is confirmed on autopsy. There is atrophy of some of the gyri (folds) of the cerebral cortex and the hippocampus, an important center of memory. Nerve cells exhibit neurofibrillary tangles— dense masses of broken and twisted cytoskeleton (fig. 12.28). These were first observed by Alois Alzheimer in 1907 in the brain of a patient who had died of senile dementia. The more severe the disease symp-

Figure 12.28 Cerebral Tissue from a Person with Alzheimer Disease. Neurofibrillary tangles appear within the neurons, and a senile plaque is evident in the extracellular matrix.

toms, the more neurofibrillary tangles are seen at autopsy. In the intercellular spaces, there are senile plaques consisting of aggregations of cells, altered nerve fibers, and a core of p-amyloid protein—the breakdown product of a glycoprotein of plasma membranes. p-amyloid protein is rarely seen in elderly people without AD.

AD is marked by the degeneration of cholinergic neurons and a deficiency of ACh. Treatment with ACh precursors is ineffective, but therapy with cholinesterase inhibitors to slow down the degradation of existing ACh has been of some value. AD patients show a deficiency of nerve growth factor (NGF; see insight 12.3) in some regions of the brain. NGF stimulates ACh synthesis; it helps to retard brain degeneration in humans and other animals and improves memory in some AD patients. Intense biomedical research efforts are currently geared toward identifying the cause of AD and developing treatment strategies. Researchers have identified three genes on chromosomes 1, 14, and 21 for various forms of early- and late-onset AD.

Parkinson30 disease (PD), also called paralysis agitans or parkinson-ism, is a progressive loss of motor function beginning in a person's 50s or 60s. It is due to degeneration of dopamine-releasing neurons in a portion of the brain called the substantia nigra. A gene has recently been identified for a hereditary form of PD, but most cases are nonhereditary and of little-known cause; some authorities suspect environmental neurotoxins.

Dopamine (DA) is an inhibitory neurotransmitter that normally prevents excessive activity in motor centers of the brain called the basal nuclei. Degeneration of the dopamine-releasing neurons leads to an excessive ratio of ACh to DA, leading to hyperactivity of the basal nuclei. As a result, a person with PD suffers involuntary muscle contractions. These take such forms as shaking of the hands (tremor) and compulsive "pill-rolling" motions of the thumb and fingers. In addition, the facial muscles may become rigid and produce a staring, expressionless face with a slightly open mouth. The patient's range of motion diminishes. He or she takes smaller steps and develops a slow, shuffling gait with a forward-bent posture and a tendency to fall forward. Speech becomes slurred and handwriting becomes cramped and eventually illegible. Tasks such as buttoning clothes and preparing food become increasingly laborious.

Patients cannot be expected to recover from PD, but its effects can be alleviated with drugs and physical therapy. Treatment with dopamine is ineffective because it cannot cross the blood-brain barrier, but its precursor, levodopa (l-DOPA), does cross the barrier and has been used to treat PD since the 1960s. l-DOPA affords some relief from symptoms, but it does not slow progression of the disease and it has undesirable side effects on the liver and heart. It is effective for only 5 to 10 years of treatment. A newer drug, Deprenyl, is a monoamine oxidase (MAO) inhibitor that retards neuronal degeneration and delays the development of symptoms. Modest improvement has been obtained by implanting other dopamine-producing tissues into the brains of PD patients—namely, adrenal medulla and fetal brain tissue. Even though the latter tissue has not come from elective abortions, this approach has triggered ethical controversy.

A surgical technique called pallidotomy has been used since the 1940s to alleviate severe tremors. It involves the destruction of a small portion of cerebral tissue in an area called the globuspallidus. Pallidotomy fell out of favor in the late 1960s when l-DOPA came into common use. By the early 1990s, however, the limitations of l-DOPA had become apparent, while MRI- and CT-guided methods had improved surgical precision and reduced the risks. Pallidotomy has thus made a comeback. Other surgical treatments for parkinsonism target brain areas called the subthalamic nucleus and the ventral intermediate nucleus of the thalamus, and involve either the destruction of tiny areas of tissue or the implantation of a stimulating electrode.

29Alois Alzheimer (1864-1915), German neurologist

30James Parkinson (1755-1824), British physician

Inflammatory Tangle

Figure 12.28 Cerebral Tissue from a Person with Alzheimer Disease. Neurofibrillary tangles appear within the neurons, and a senile plaque is evident in the extracellular matrix.

Saladin: Anatomy & I 12. Nervous Tissue I Text I I © The McGraw-Hill

Physiology: The Unity of Companies, 2003 Form and Function, Third Edition

476 Part Three Integration and Control

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