Parkinson’s Disease and the protective mechanism of the antioxidant Vitamin E
Description and Risks
Parkinson’s disease (PD) is a progressive movement disorder marked by tremors, rigidity, slow movements (bradykinesia), and postural instability. It is a chronic, progressive neurodegenerative disease caused by decreased production of dopamine, a neurotransmitter. Dopamine is responsible for most of the body’s smooth muscle movements. As a result, motor control in Parkinson’s patients is disrupted, causing anything from uncontrollable tremors to muscular stiffness to slow-as-molasses movements. (2) PD affects about 500,000 people in the United States, both men and women, with as many as 50,000 new cases each year. The disease usually begins in a person’s late 50’s and 60’s; it causes a progressive decline in movement control, affecting the ability to control initiation, speed, and the smoothness of motion. The symptoms of PD are seen in up to 15% of those between the ages of 65-74, and almost 30% of those were between the ages of 75-84. (3)
Genetic Risks
Scientist identified two gene abnormalities present in PD patients whose families have a rate of the disease, indicating at least some evidence that the disease is inherited. Both abnormalities cause the body to produce an altered version of alpha synuclein, the protein that shows up in dense masses in the brains of Parkinson’s patients. (3). But in another study in the Journal of the American Medical Association suggested heredity is a significant influence on how fast the disease will onset. Researchers identified 172 twin pairs in which at least one twin had PD. If the condition was hereditary, the rate of both twins having the disease would be lower among fraternal twins, who share some, but not all of the same genes unlike identical twins who share them all. In individuals who were diagnosed after age 50, the rate of twins who both had the disease was similar among fraternal and identical twins. In those diagnosed at 50 or younger, however, the rate was significantly lower in fraternal twins than in identical twins (2). Researchers also think that PD has environmental risks such as increase exposure to toxic chemicals such as pesticides, herbicides, or heavy metals. For example, some studies of people liv...
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...one, L., Bagala, A., Napoli, I.D., Caracciolo, M. & Quattnone, A. (2001) Plasma levels of Vitamin E in Parkinson’s disease. Archives of Gerontology and Geriatrics 33:7-12.
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10. Parashevas, G.P., Kapaki, E., Petropoulou, O., Anagnostouli, M., Vagenas, V. & Papageorgiou, L. (2003) Plasma levels of Antioxidant Vitamins C and E are decreased in vascular Parkinsonism. Journal or Neurological Sciences. 215:51-55.
11. Roghani, M. & Behzadi, G., (2001) Neuroprotective effect of vitamin E on the early model of Parkinson’s disease in rat: behavioral and histochemical evidence. Brain Research 892:211-217.
12. Vatassery, G.T., Demaster, E.G., Lai, James C.K., Smith, W.E. & Quach, H.T. (2003) Iron uncouples oxidative phosphorylation in brain mitochondria isolated from vitamin E-deficient rats. Biochemical et Biophysical Acta 1688:265-273.
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"About Parkinson's Disease." Research Is The Key to A Cure. The Michael Stern Research Foundation, n.d. Web. 10 Jan 2014. .
People who have been diagnosed with this lifelong disease have either started to see the early signs and symptoms or have yet to recognize them. The negative impact that fatigue, loss of muscle strength and in-coordination has on the patients with Parkinson’s disease can be improved with a well-balanced exercise regimen. The three most common physical symptoms the patient will experience are tremors, rigidity, and bradykinesia. “Tremors while at rest are the most common initial symptom and are present in around 70 percent of cases at disease onset. It often presents as a pill rolli...
Goldmann, David R., and David A. Horowitz. American College of Physicians Home Medical Guide to Parkinson's Disease. New York: Dorling Kindersley Pub., 2000. Print.
With more than 200,000 US cases per year, Parkinson’s disease has become a major part
The path physiology of Parkinson’s disease is the pathogenesis if Parkinson disease is unknown. Epidemiologic data suggest genetic, viral, and environmental toxins as possible causes. Nigral and basal loss of neurons with depletion of dopamine, an inhibitory neurotransmitter, is the principal biochemical alteration in Parkinson disease. Symptoms in basal ganglia disorders result from an imbalance of dopaminergic (inhibitory) and cholinergic (excitatory) activity in the caudate and putamen of the basal ganglia.
Parkinson's is an idiopathic, multifactorial neurodegenerative disease that attacks neurotransmitters in the brain called dopamine. Dopamine is concentrated in a specific area of the brain called the substantia nigra. The neurotransmitter dopamine is a chemical that regulates muscle movement and emotion. Dopamine is responsible for relaying messages between the substantia nigra and other parts of the brain to control body movement. The death of these neurotransmitters affects the central nervous system. The most common symptoms are movement related, including shaking, rigidity, slowness of movement and difficulty with posture. Behavioral problems may arise as the disease progresses. Due to the loss of dopamine, Parkinson's patients will often experience depression and some compulsive behavior. In advanced stages of the disease dementia will sometimes occur. The implications of the disease on the anatomy and physiology of the respiratory and phonatory systems significantly control speech.
“An Examination of Animal Experiments.” Physician Committee for Responsible Medicine. N.p., n.d. Web. 13 Feb. 2014. .
Parkinson’s disease is a chronic, progressive neurodegenerative disorder characterised by resting tremor, slowed movements, rigidity and postural instability (Casey G, 2013). It is the second most common neurodegenerative disorder after Alzheimer’s (Martin and Mills, 2012). There is a great variability in reported incidence rates, probably due to difference in diagnostic criteria and case ascertainment, with reported rates in Australia and in Western countries ranging from 8.6 to 19.0 per 100,000 population (J Macphee and D Stewart, 2012). The two main brain structures affected by Parkinson’s are the substantia nigra pars compacta, which is located in the midbrain and other parts of the basal ganglia, w...
Most signs and symptoms of Parkinson disease correspond to one of three motor deficiencies: bradykinesia, akinesia, tremor, and rigidity. The first two qualities are usually present before tremor, but often attributed to aging by the patient and even the physician, and thus the disease is rarely diagnosed until tremor becomes evident much later. An average of 80% of the nigrostriatal neurons may have already degenerated by the time Parkinsonism is diagnosed, which complicates treatment (Fitzgerald, 130). Bra...
716). Characteristic features of Parkinson's disease include “motor impairment (bradykinesia, rigidity, tremor, gait dysfunction, and postural instability), cognitive impairment (frontal lobe executive dysfunction), and mood disorders” (p. 716). Normally, motor performance depends on the interaction between automatic (unconscious) and volitional (cognitive) control of movement, however those with Parkinson's disease, experience an “early and preferential loss of dopamine in the caudal regions of the basal ganglia (dorsal regions in rodents), which leads to diminished automatic and increased cognitive control of movements that include frontal lobe circuitry” (p. 716). Consequently, those with Parkinson’s disease must sustain a larger cognitive load to execute either motor or cognitive tasks, such as working memory. In the past decade, increasing evidence has accrued for the role of exercise in the improvement of motor performance, which may help both the cognitive and automatic control of movement. Thus, exercise interventions can help those with Parkinson’s disease incorporate goal-based motor skill training, which then helps in engaging circuitry important in motor learning. Individuals with Parkinson's disease become cognitively engaged with the practice and acquiring of movements and skills that were formerly automatic and unconscious. In addition, aerobic exercise is also observed as important for improvement of blood flow and assistance of neuroplasticity in the elderly, which may also play a role in the improvement of behavioral function in those with Parkinson's disease. Petzinger et al. additionally states that exercise also uses goal-based training and aerobic activity which can improve “both cognitive and automatic
Parkinson's Disease has caused problems for many people in this world and plagued the elderly all over the world.Parkinson's disease still puzzles doctors and the causes are unknown. It is known that it is a non-communicable disease and may even be hereditary. Parkinson's disease is thought to be caused by external factors. Most of the cases of this disease are caused by progressive deterioration of the nerve cells, which control muscle movement. Dopamine, one of the substances used in the brain to transmit impulses, is produced in the area of deterioration.
The mitochondria is an organelle which is generally an oval shape and is found inside the cytoplasm and is again apart of the eukaryotic cells. The main function of the mitochondria is to complete cellular respiration; in simple terms it acts like a digestive system to break down essential nutrients and to convert it into energy. This energy is usually found to in ATP which is a rich molecule taken from the energy stored in food. Furthermore, mitochondria stores calcium for signalling activities; such as heat, growth and death. They have two unique membranes and mitochondria isn’t found in human cells like the red blood cells yet liver and muscle cells are filled entirely with mitochondria.
...W.H Kwok, D.K.K Leung, T.S.M Wan, and A.S.Y Wong. "Metabolic Studies of Turinabol in Horses."Analytica Chimica Acta. 586 (2007): 208-216. Print.
"Secondary Parkinsonism: MedlinePlus Medical Encyclopedia." U.S National Library of Medicine. U.S. National Library of Medicine, n.d. Web. 11 May 2014.