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166 The neurodegenerative diseases seem to have in common a free-radical-mediated destruction of cellular components, particularly cell membranes. All seem to have inflammation involved. Apoptosis is also prevalent in most of these diseases, but this programmed or systematic suicide of cells appears to be a mechanism for preserving the organism when there is damage to specific cells. The cause of damage is not known for certain in these diseases, and may be multifactorial. In some cases, genetics plays a major role (as in multiple sclerosis and Huntington’s disease), whereas in others the genetic link seems to be a minor risk factor and environmental factors are perhaps making more significant contributions. Multiple Sclerosis Multiple sclerosis (MS) is one of the most common autoimmune neurodegenerative disorders. T lymphocytes cross the blood-brain barrier and attack oligodendrocytes, destroying the myelin sheath that surrounds long axonal projections in the central nervous system. The destruction of myelin and its accompanying inflammation disrupt nerve impulses, all of which become most prevalent during a relapse. There may be some repair of damaged tissue as well as suppression of inflammation during the remission phase. Over time, however, the damage that accrues during relapses may become extensive and result in considerable loss of function. The overt symptoms of MS can vary widely from one individual to another. There is generally muscle weakness, which leads to decreased mobility and often results in bladder instability. Difficulty in chewing and swallowing can lead to malnutrition. There is much anecdotal evidence that diet can influence the course of MS, although reviews of dietary intervention trials to manage the progression of MS have been discouraging. 13 Neurodegenerative Diseases 166 NEURODEGENERATIVE DISEASES 167 Epidemiology studies indicate that countries with high saturated fat intake have higher incidence of MS than those with higher PUFA intake (Payne 2001), although such gross associations need more careful scrutiny. The rate of MS in Switzerland is inversely associated with altitude of residence, whereas in Norway there is a higher prevalence of MS inland than along the coast (Hayes, Cantorna, and DeLuca 1997). The Norwegian phenomenon has been used to argue that omega-3 fish oils may be beneficial in suppressing MS. The Swiss phenomenon has been explained by higher levels of vitamin D (the sunshine vitamin) in the population at higher altitudes as a result of greater UV light intensity. The latter explanation is further supported by the rarity of MS in the tropics and the dramatic increase in incidence with higher latitude in both Northern and Southern hemispheres. One study found a large (38 percent) increase in lipid peroxidation and other markers of oxidative stress in MS patients versus controls (Karg et al. 1999). Lipid peroxides are generally elevated when increased immune system activity and inflammation are present. Antioxidant vitamins are often recommended for MS, although clinical trials for such intervention have given mixed results. There is a sound basis for omega-3, particularly DHA, supplements. It was mentioned (in chapter 11) that DHA supplements increased levels of plasmalogens , which have antioxidant properties and are normally at high levels in myelin. The arguments regarding vitamin D suggest that calcium is important, along with vitamin D. However, vitamin D could be affecting MS in ways that do not involve calcium. In view of the limited information currently available, it seems that adequate amounts of omega-3 oils, vitamins, and minerals, particularly vitamin D and calcium, may be a good approach to slow the progress of this devastating disease. Amyotrophic Lateral Sclerosis Amyotrophic lateral sclerosis (ALS) is characterized by progressive loss of motor neurons, particularly in the spinal cord. Patients typically succumb to the disease within five years of onset. As with some other neurodegenerative diseases, there is a small (5 to 10 percent) chance of it being genetic; the majority of ALS cases are considered to be idiopathic. Hereditary ALS has been associated with several genes. The gene for copper-zinc superoxide dismutase (SOD1) on chromosome 21 has received the most attention, but only about one in every five or six cases of familial ALS is associated with mutations in the SOD1 gene. A transgenic mouse model has been developed using a mutant SOD1 gene that mimics several characteristics of the human disease. This lends support to the hypothesis that free radicals and reactive oxygen species are important components of the neurodegenerative process, and may be generated by an inflammatory immune response (Emerit, Edeas, and Bricaire 2004...

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