Parkinson's disease

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Parkinson's disease could be prevented by simply eating less. Intermittent fasting or caloric restriction may help. 
Experimental and clinical evidence:

Extract from recent article: Dietary restriction in cerebral bioenergetics and redox state
Ignacio Amigo and Alicia J. Kowaltowski
Redox Biol. 2014; 2: 296–304, Published online Jan 11, 2014. doi:  10.1016/j.redox.2013.12.021
PMCID: PMC3926116

Another well-known neurodegenerative condition is Parkinson’s disease (PD), which causes progressive motor dysfunction due to selective loss of dopaminergic neurons from the substantia nigra that project to the striatum. In addition, accumulation of Lewy bodies containing aggregated proteins such as α-synuclein, increased inflammation, mitochondrial dysfunction and oxidative imbalance are all common features observed [54].

Mitochondrial alterations in PD include increased mitochondrial permeability transition pore opening, loss of NAD, defective mitochondrial dynamics and impaired clearance of damaged mitochondria, leading to accumulation of mitochondrial DNA mutations and high ROS levels. PD-linked mutations in genes that codify for mitochondrial proteins include PINK1, parkin, and LRRK2 [95,24].

Several models are used to study PD, including α-synuclein mutant mice, which develop a degenerative condition similar to PD in humans, and administration of rotenone or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which induce a parkinsonian phenotype by impairing mitochondrial complex I activity [15].

Mice on an IF diet are protected against neuronal loss in the substantia nigra and show improved motor function after MPTP administration [34]. The same diet has shown beneficial effects even when started after MPTP administration, decreasing the extracellular levels of striatal glutamate [53]. In addition, reports indicate that IF can alleviate some of the collateral effects of PD, such as the elevated heart rate in a mouse model of α-synuclein accumulation [46] and the high levels of circulating corticosterone, which are detrimental for neuronal viability and plasticity [88]. However, the same diet was ineffective in rats against nigrostriatal degeneration induced by 6-hydroxydopamine, an alternative model for PD [4]. Interestingly, a study carried out in primates indicates that a 30% CR diet prior to MPTP administration increases the level of neurotrophic factors in the brain, improves motor activity and reduces the loss of dopamine and its related metabolites [68].

Recent evidence indicates that the gastrointestinal system could play a noted role in the development of PD and that the orexigenic signal ghrelin, which is produced in the stomach in response to fasting and whose levels are increased during dietary restriction, could be neuroprotective [9].

Parkinson's diseases could be prevented by simply eating less, a British neuroscientist has claimed. Dr Mark Mattson, leading a scientific team in the US, found that rats fed on a low calorie diet are less affected by brain-destroying chemicals than those eating normally. It's well known that high food intake increases the risk of heart disease, diabetes and cancer, but Mattson said the findings are "the first to suggest that reduced calorie intake also may help shield the brain". In the study, reported in Annals of Neurology, one group of rats was fed 30% less food than the control group, and both were then treated with two different brain toxins. One toxin simulates brain damage found in people with Alzheimer's disease and those who've suffered a stroke. The other mimics the brain damage caused by Huntington's and Parkinson's diseases. In both cases, the rats on the low-cal diet suffered much less brain damage, with fewer memory and motor skill deficits compared with that suffered by rats on a normal diet. Dr Arthur Everitt, founder of the Australian Association of Gerentology, said the findings are consistent with previous studies showing the health benefits of caloric restriction. "It's crazy for people to allow themselves to become overweight," he said.

Caloric restriction and intermittent fasting: two potential diets for successful brain aging.
Ageing Res Rev. 2006 Aug;5(3):332-53. Epub 2006 Aug 8.
Martin B1, Mattson MP, Maudsley S.

The vulnerability of the nervous system to advancing age is all too often manifest in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. In this review article we describe evidence suggesting that two dietary interventions, caloric restriction (CR) and intermittent fasting (IF), can prolong the health-span of the nervous system by impinging upon fundamental metabolic and cellular signaling pathways that regulate life-span. CR and IF affect energy and oxygen radical metabolism, and cellular stress response systems, in ways that protect neurons against genetic and environmental factors to which they would otherwise succumb during aging. There are multiple interactive pathways and molecular mechanisms by which CR and IF benefit neurons including those involving insulin-like signaling, FoxO transcription factors, sirtuins and peroxisome proliferator-activated receptors. These pathways stimulate the production of protein chaperones, neurotrophic factors and antioxidant enzymes, all of which help cells cope with stress and resist disease. A better understanding of the impact of CR and IF on the aging nervous system will likely lead to novel approaches for preventing and treating neurodegenerative disorders.

Caloric restriction increases neurotrophic factor levels and attenuates neurochemical and behavioral deficits in a primate model of Parkinson's disease.

Proc Natl Acad Sci U S A. 2004 Dec 28;101(52):18171-6. Epub 2004 Dec 16.
Maswood N1, Young J, Tilmont E, Zhang Z, Gash DM, Gerhardt GA, Grondin R, Roth GS, Mattison J, Lane MA, Carson RE, Cohen RM, Mouton PR, Quigley C, 
Mattson MP, Ingram DK.
We report that a low-calorie diet can lessen the severity of neurochemical deficits and motor dysfunction in a primate model of Parkinson's disease. Adult male rhesus monkeys were maintained for 6 months on a reduced-calorie diet [30% caloric restriction (CR)] or an ad libitum control diet after which they were subjected to treatment with a neurotoxin to produce a hemiparkinson condition. After neurotoxin treatment, CR monkeys exhibited significantly higher levels of locomotor activity compared with control monkeys as well as higher levels of dopamine (DA) and DA metabolites in the striatal region. Increased survival of DA neurons in the substantia nigra and improved manual dexterity were noted but did not reach statistical significance. Levels of glial cell line-derived neurotrophic factor, which is known to promote the survival of DA neurons, were increased significantly in the caudate nucleus of CR monkeys, suggesting a role for glial cell line-derived neurotrophic factor in the anti-Parkinson's disease effect of the low-calorie diet.

Dietary restriction and 2-deoxyglucose administration improve behavioral outcome and reduce degeneration of dopaminergic neurons in models of Parkinson's disease.

Duan W1, Mattson MP. J Neurosci Res. 1999 Jul 15;57(2):195-206.

Parkinson's disease (PD) is an age-related disorder characterized by progressive degeneration of dopaminergic neurons in the substantia nigra (SN) and corresponding motor deficits. Oxidative stress and mitochondrial dysfunction are implicated in the 
neurodegenerative process in PD. Although dietary restriction (DR) extends lifespan and reduces levels of cellular oxidative stress in several different organ systems, the impact of DR on age-related neurodegenerative disorders is unknown. We report that DR in adult mice results in resistance of dopaminergic neurons in the SN to the toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). MPTP-induced loss of 
dopaminergic neurons and deficits in motor function were ameliorated in DR rats. To mimic the beneficial effect of DR on dopaminergic neurons, we administered 2-deoxy-D-glucose (2-DG; a nonmetabolizable analogue of glucose) to mice fed ad libitum. Mice receiving 2-DG exhibited reduced damage to dopaminergic neurons in the SN and improved behavioral outcome following MPTP treatment. The 2-DG treatment suppressed oxidative stress, preserved mitochondrial function, and attenuated cell death in cultured dopaminergic cells exposed to the complex I inhibitor rotenone or Fe2+. 2-DG and DR induced expression of the stress proteins heat-shock protein 70 and glucose-regulated protein 78 in dopaminergic cells, suggesting involvement of these cytoprotective proteins in the neuroprotective actions of 2-DG and DR. The striking beneficial effects of DR and 2-DG in models of PD, when considered in light of recent epidemiological data, suggest that DR may prove beneficial in reducing the incidence of PD in humans.
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