Calorie restriction protects primates from Parkinsons disease

December 13, 2004 Printer Friendly
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Calorie restriction protects primates from Parkinson’s disease


Parkinson’s disease

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Calorie restriction protects primates from Parkinson’s disease
In a study that will appear this week in the online early edition of The Proceedings of the National Academy of Sciences, Donald K. Ingram of the National Institute on Aging and colleagues have found that long-term calorie restriction protects monkeys from developing Parkinson’s disease.

Calorie restriction involves a significant reduction in the intake of energy from the diet, and has been found to reduce the signs of aging and extend lifespan in many different species. Because Parkinson’s disease involves an acceleration of the loss of dopamine neurons in the substantia nigra of the brain that occurs with “normal” aging, a technique that slows aging could impact the development of the disease.

Six rhesus monkeys were provided with a control diet, and seven were fed a diet that was 30 percent lower in calories but otherwise identical to the control diet for six months, after which both groups were injected with a neurotoxin that causes Parkinson-like disease. PET scans were performed 1 to 3 weeks prior to and 12 to 16 weeks following the neurotoxin administration. The animals’ behavior was observed and assessed for the following 16 to 18 weeks.

The researchers found that calorie restricted monkeys exhibited greater locomotor activity than animals who received the control diet. Brain tissue samples obtained 16 to 18 weeks following treatment with the neurotoxin revealed higher levels of dopamine and dopamine metabolites in the restricted animals, and increased levels of the glial cell line-derived neurotrophic factor (GDNF), which promotes the survival of dopamine neurons.

An accompanying editorial, Caleb E Finch of the University of Southern California in Los Angeles discusses the possible protective mechanisms of calorie restriction against the development of Parkinson’s disease. The reduction of oxidative stress that results when calorie restriction is adopted as well as the induction of heat shock chaperones that protect the cells may reduce neurotoxicity resulting from exposure to various compounds. Dr Finch asks whether the increased physical activity that has been observed in calorie restricted animals could be responsible for the neuroprotection observed in this and other studies, noting that exercise in rodent studies has been associated with an increase in brain-derived neurotrophic factor. He explains that hunger may increase locomotor activity as an adaptive foraging behavior. He also notes the possible consequences of toxins stored in fat, and reiterates the authors’ remarks that a low fat intake and body mass index appear to lower the risk of Parkinson’s disease.


Parkinson’s disease
Parkinson's disease (also called paralysis agitans) is a degenerative central nervous system disorder. Parkinson's disease is generally a disease of unknown cause, affecting persons over the age of 60 (Glanze 1996). In the United States, about 1% of individuals (1 in 200) over the age of 60 are affected (Clayman 1989). However, the disease may occur in younger persons, particularly following inflammation of the brain (encephalitis) or from poisoning by carbon monoxide, metals, or certain drugs. Men are more likely to be affected than women. Interestingly, incidence of Parkinson's disease is lower in smokers (Glanze 1996).

The symptoms of Parkinson's disease are attributed to a loss of brain cells in the basal ganglia (Clayman 1989). These cells produce the neurotransmitter dopamine. There also seem to be abnormalities in other parts of the brain and in the availability of other neurotransmitters, such as serotonin and nor-epinephrine (Adam et al. 1983; Kish et al. 1984; Stern et al. 1984; Taylor et al. 1986; Ring et al. 1994; Arahata 1999; Bohnen et al. 1999; Narabayashi 1999).

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).

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Research indicates that deprenyl is probably even more effective in preventing Parkinson's disease that in treating it, and suggests several mechanisms of action by which deprenyl can rescue dying neurons (brain cells).

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If you have questions or comments concerning this issue or past issues of Life Extension Update, send them to or call 954 766 8433 extension 7716.

For longer life,

Dayna Dye
Editor, Life Extension Update
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