Academic journal article Generations

Parkinson's Disease in Later Life

Academic journal article Generations

Parkinson's Disease in Later Life

Article excerpt

Parkinson's disease was first described by Dr. James Parkinson in his 1817 monographylw Essay on the Shaking Palsy.

His initial description of a "relentlessly progressive" disease characterized by tremor, gait disturbance, slowness of movement, and disturbed sleep remains valid today (Parkinson, 1817). The clinical progression was delineated further by Jean-Martin Charcot at Salpetriere Hospital in Paris. However, the hallmark of the diseaseloss of brainstem cells that produce dopamine (a neurotransmitter) -was not discovered until the middle of the last century (Fahn, 2003; Hornykiewicz, 2001). The diagnosis of Parkinson's disease is still based on physical examination and history rather than on brain imaging or laboratory tests (Tarsy, 2005). The underlying cause of the disease continues to elude researchers.

Parkinson's disease affects approximately million people in the United States (Tanner and Aston, 2000). Its presence in the public consciousness is larger because of high-profile patients like the late Pope John Paul II, the actor Michael J. Fox, and Muhammed AIi. The average age of onset is late in the sixth decade of life, and prevalence increases with age. According to one study, Parkinson's disease affects 0.3 percent of people age 55 to 64, 1 percent of people age 65 to 74, 3.1 percent of people age 75 to 84, and 4.3 percent of people age 85 to 94 (De Rijk et al., 1995). The ratio of males to females is three to two, but this difference appears to dissipate later in life. The prevalence and incidence of the disease in terms of race/ethnicity remain controversial. While some studies suggest a lower prevalence in people of African ancestry (Cosnett and Bill, 1988), others have suggested either a higher incidence (Mayeux et al., 1995), or no difference within the U.S. population (Louis et al., 1996; McInerney-Leo, Gwinn-Hardy, and Nussbaum, 2004). The prevalence among Asian (Tan et al., 2004; Wang et al., 1996) and Hispanic populations is also uncertain but is probably similar to prevalence in Caucasians (Louis et al., 1996; Marder et al., 1998).

Epidemiological studies have investigated factors that may cause Parkinson's disease, but the studies have yet to identify definitive correlations. While Parkinson's disease is generally more common in industrialized societies, it is found with greater frequency in rural areas (Marder et al., 1998). Exposure to pesticides and drinking well water have been postulated as risk factors. Laboratory rats developed signs of parkinsonism after they were given large doses of the pesticide rotenone (Alam and Scnmidt, 2002). Paradoxically, though, rotenone is allowed in organic farming practices, and typical exposure rates have not been shown to cause Parkinson's disease. No specific environmental agent has been shown to cause Parkinson's disease in people.

Researchers have been intrigued by negative correlations of Parkinson's disease with exposure to cigarettes and coffee (Tan et al., 2003). It is not dear whether these agents are protective or whether early changes in dopamine-mediated reward systems in the brains of people destined to develop Parkinson's disease make them less susceptible to the addictive qualities of nicotine and caffeine. We certainly do not suggest taking up smoking and coffee-drinking as preventive measures.

Despite the elusiveness of the underlying cause of Parkinson's disease, scientists have discovered much about the pathological changes that the disease induces in the brain. In Parkinson's disease, dopamine-producing cells in the brainstem become gradually depleted. This deficit leads to malfunction of dopamine-dependent pathways for the initiation and control of voluntary movements. However, it is not simply a disease of dopamine deficiency; other neurotransmitters (serotonergic and noradrenergic systems) are also affected. Recent evidence suggests that pathological changes begin in the spinal cord and brainstem and gradually ascend to involve higher brain structures, including the cerebral cortex (Braak et al. …

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