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Selegiline may be one of the best treatments for early Parkinson’s disease
The meta-analysis included 17 trials involving 3,525 patients with Parkinson’s disease. Thirteen trials compared selegiline with a placebo or with levodopa, a drug that most patients with Parkinson’s disease eventually need. The four remaining trials involved other MAOBIs. Some of the trials compared the effects of a combination of a MAOBI and levodopa to a placebo with or without levodopa.
The researchers, from the University of Birmingham in England, found that participants who received MAOBIs had significantly less disability compared to those who received placebos. Patients on MAOBIs also experienced a delay in the need for levodopa, and those using the drug were less likely to require increased amounts. Additionally, those receiving MAOBIs had a reduced risk of developing motor fluctations. No substantial side effects or increased mortality were found in those taking MAOBIs.
This meta-analysis is the first to evaluate MAOBIs as a drug class for early Parkinson’s disease. The authors conclude, “Our review provides no evidence that mortality is increased by selegiline and suggests that this inexpensive drug could be one of the most clinically effective and cost effective treatments available for early Parkinson’s disease.”
The most commonly used levodopa drug is Sinemet. Sinemet contains the decarboxylase inhibitor carbidopa to prevent deactivation of L-dopa before it reaches the brain.
Eldepryl (deprenyl) is a selective monoamine oxidase inhibitor (MAOI) that slows the breakdown of dopamine in the brain, thereby initially reducing the need for levodopa by up to 30%. This effect diminishes with time. Therefore, in the early stages of Parkinson's disease, Eldepryl alone may alleviate symptoms. Eldepryl is also used in combination with Sinemet, particularly when Sinemet no longer seems to be working well. At this stage, Eldepryl has no effect when taken by itself and works only in combination with Sinemet (PDR 2002). Deprenyl and selegiline hydrochloride are generic names for Eldepryl.
There is some evidence that the generic drug deprenyl has a protective effect on brain cells when compared to levodopa, which appears to lead to more rapid deterioration (Mytilineou et al. 1993; Tipton 1994; Pardo et al. 1995; Wu et al. 1995; Liou et al. 2001). While deprenyl has received some bad publicity in recent years, it is now clear that deprenyl is safe in combination with levodopa.
Supplementation with nutrients has reported benefits for persons with Parkinson's disease. These supplements include amino acids, antioxidants, coenzyme Q10, melatonin, folic acid, acetyl-L-carnitine, octacosanol, phosphatidylserine, NADH, and the European drug Hydergine (Snider 1984; Yapa 1992; Mizuta et al. 1993; Schulz et al. 1995; 1996; Shults et al. 1997; 1998; 1999; Beal et al. 1998; Golbe et al. 1998; Sakagami et al. 1998; Seitz et al. 1998; Beal 1999; Jimenez-Jimenez et al. 2000; Kidd 2000; Nadlinger et al. 2001; Roghani et al 2001; Ross 2001; Tan et al. 2001; Zisapel 2001; Antolin et al. 2002; Chen et al. 2002; Duan et al. 2002).
Coenzyme Q10 (coQ10) has long been considered an essential nutrient for cardiac health because of its role in boosting cellular energy. When coQ10 is orally administered, it works its way into the cells' mitochondria (the cells' powerhouses) where it helps to convert fats and sugars into energy. Thus, scientists have focused on its critical role in heart function. But, further studies have identified coQ10's other important role: as a neuroprotective agent.
It is a fact that coQ10 diminishes with age. This means mitochondrial energy decreases accordingly, leading to what is now being referred to as “mitochondrial disorders” or simply put, suboptimal health, as cellular energy and function are compromised.
Brain tissues are especially rich in phosphatidylserine (PS), but aging causes a decline in the PS content of cells throughout the body. Research has shown that in addition to improving neural function, PS enhances energy metabolism in all cells. In the brain, PS helps maintain cell membrane integrity and youthful synaptic plasticity.
In a study of Parkinson’s disease patients, 360 mg a day of coQ10 was administered for only four weeks, producing a mild symptomatic improvement compared to placebo. More important, an established clinical test to measure Parkinson’s symptom function showed significantly better improvement of performance in the coQ10-supplemented patients compared with the placebo group.
This new study helped to corroborate a report last year that Parkinson’s patients consuming 1200 mg a day of coQ10 showed a 44% reduction in the decline of motor skills, movement, and mental function compared to the placebo group. Those receiving this high-dose coQ10 also demonstrated an improved ability to perform daily living tasks. This 16-month study was remarkable in that coQ10 slowed the progression of the disease, something that Parkinson’s drugs do not do.
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