enfermedades neurodegenerativas


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La enfermedades neurodegenerativas pueden ser ralentizadas e incluso revertidas mediante el ayuno y la restricción calórica. Mirar aquí la evidencia científica:

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 B, Mattson MP, Maudsley S.

Caloric restriction improves memory in elderly humans
Proc Natl Acad Sci U S A. 2009 Jan 27;106(4):1255-60. Epub 2009 Jan 26
Witte AV, Fobker M, Gellner R, Knecht S, Flael A.
Department of Neurology, University of Munster, Albert-Schweitzer-Strasse 33, 48149 Munster, Germany.
Animal studies suggest that diets low in calories and rich in unsaturated fatty acids (UFA) are beneficial for cognitive function in age. Here, we tested in a prospective interventional design whether the same effects can be induced in humans. Fifty healthy, normal- to overweight elderly subjects (29 females, mean age 60.5 years, mean body mass index 28 kg/m(2)) were stratified into 3 groups: (i) caloric restriction (30% reduction), (ii) relative increased intake of UFAs (20% increase, unchanged total fat), and (iii) control. Before and after 3 months of intervention, memory performance was assessed under standardized conditions. We found a significant increase in verbal memory scores after caloric restriction (mean increase 20%; P < 0.001), which was correlated with decreases in fasting plasma levels of insulin and high sensitive C-reactive protein, most pronounced in subjects with best adherence to the diet (all r values < -0.8; all P values <0.05). Levels of brain-derived neurotrophic factor remained unchanged. No significant memory changes were observed in the other 2 groups. This interventional trial demonstrates beneficial effects of caloric restriction on memory performance in healthy elderly subjects. Mechanisms underlying this improvement might include higher synaptic plasticity and stimulation of neurofacilitatory pathways in the brain because of improved insulin sensitivity and reduced inflammatory activity. Our study may help to generate novel prevention strategies to maintain cognitive functions into old age.
Full article available with subscription - PNAS

Neurodegenerative Diseases and Fasting

Brain disorders such as Alzheimer's and 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.

Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems.
J Nutr Biochem. 2005 Mar;16(3):129-37.
Mattson MP, Wan R.
Laboratory of Neurosciences, National Institute on Aging Intramural Research Program, Baltimore, MD 21224.Intermittent fasting (IF; reduced meal frequency) and caloric restriction (CR) extend lifespan and increase resistance to age-related diseases in rodents and monkeys and improve the health of overweight humans. Both IF and CR enhance cardiovascular and brain functions and improve several risk factors for coronary artery disease and stroke including a reduction in blood pressure and increased insulin sensitivity. Cardiovascular stress adaptation is improved and heart rate variability is increased in rodents maintained on an IF or a CR diet. Moreover, rodents maintained on an IF regimen exhibit increased resistance of heart and brain cells to ischemic injury in experimental models of myocardial infarction and stroke. The beneficial effects of IF and CR result from at least two mechanisms--reduced oxidative damage and increased cellular stress resistance. Recent findings suggest that some of the beneficial effects of IF on both the cardiovascular system and the brain are mediated by brain-derived neurotrophic factor signaling in the brain. Interestingly, cellular and molecular effects of IF and CR on the cardiovascular system and the brain are similar to those of regular physical exercise, suggesting shared mechanisms. A better understanding of the cellular and molecular mechanisms by which IF and CR affect the blood vessels and heart and brain cells will likely lead to novel preventative and therapeutic strategies for extending health span.

Redefining neuroprotective gene therapeutic strategies: Lessons learned from caloric restriction and NAD(+) metabolism.
J Alzheimers Dis. 2004 Dec;6(6 Suppl):S43-6.
Henricksen LA, Federoff HJ.
Center for Aging and Developmental Biology, Aab Institute for Biomedical Sciences, Universityof Rochester Schoolof Medicineand Dentistry, Rochester, MN.
Herein a case is made for the development of novel cytoprotective approaches based upon molecular mechanisms thought to underlie the caloric restriction phenomenon. This analysis leads to the prediction that molecular genetic perturbations affecting the metabolism of nuclear NAD(+) and metabolites will be neuroprotective.

An HPLC tracing of the enhancer regulation in selected discrete brain areas of food-deprived rats.
Life Sci 2003 May 9;72(25):2923-30
Miklya I, Knoll B, Knoll
J. Neuropsychopharmacological Research Unit of the Hungarian Academy of Sciences, P.O.B. 370, H-1445, Budapest, Hungary.
The recent discovery of the enhancer regulation in the mammalian brain brought a different perspective to the brain-organized realization of goal-oriented behavior, which is the quintessence of plastic behavioral descriptions such as drive or motivation. According to this new approach, 'drive' means that special endogenous enhancer substances enhance the impulse-propagation-mediated release of transmitters in a proper population of enhancer-sensitive neurons, and keep these neurons in the state of enhanced excitability until the goal is reached. However, to reach any goal needs the participation of the catecholaminergic machinery, the engine of the brain. We developed a method to detect the specific enhancer effect of synthetic enhancer substances [(-)-deprenyl, (-)-PPAP, (-)-BPAP] by measuring the release of transmitters from freshly isolated selected discrete brain areas (striatum, substantia nigra, tuberculum olfactorium, locus coeruleus, raphe) by the aid of HPLC with electrochemical detection. To test the validity of the working hypothesis that in any form of goal-seeking behavior the catecholaminergic and serotonergic neurons work on a higher activity level, we compared the amount of norepinephrine, dopamine, and serotonin released from selected discrete brain areas isolated from the brain of sated and food-deprived rats. Rats were deprived of food for 48 and 72 hours, respectively, and the state of excitability of their catecholaminergic and serotonergic neurons in comparison to that of sated rats was measured. We tested the orienting-searching reflex activity of the rats in a special open field, isolated thereafter selected discrete brain areas and measured the release of norepinephrine, dopamine, and serotonin from the proper tissue samples into the organ bath. The orienting-searching reflex activity of the rats increased proportionally to the time elapsed from the last feed and the amount of dopamine released from the striatum, substantia nigra and tuberculum olfactorium, that of norepinephrine released from the locus coeruleus and that of serotonin released from the raphe increased significantly in the hungry rats proportionally to the time of fasting. For example: the amount of dopamine released from the substantia nigra of sated rats (4.62 +/- 0.20 nmoles/g wet weight) increased to 5.95 +/- 0.37 (P < 0.05) and 10.67 +/- 0.44 (P < 0.01) in rats deprived of food for 48 and 72 hours, respectively.


Effects of Age and Dietary Restriction on Lifespan and Oxidative Stress of SAMP8 Mice with Learning and Memory impairments.
J Nutr Health Aging 2000;4(3):182-186
Choi J, Kim D.
Faculty of Food Science and Biotechnology, Pukyong National University; 599-1 Daeyeon-Dong, Nam-Gu, Pusan 608-737, Korea.
This study was to evaluate the effect of dietary restriction (DR) on lifespan and oxidative stress of dementia mouse model SAMP8 with impaired learning and memory. SAMP8 female mice were fed either ad libitum (AL) or fed 60% of food intake of AL. Results showed that basal metabolic rates (BMR) were significantly lower (15 to 22%) in DR with increased median and maximum lifespans, suggesting feed and gross efficiencies were significantly lower in DR than in AL. Grading score of senescence resulted in a marked improvement about 2-fold by DR compared with AL. The amounts of lipofuscin at 12 months were significantly lowered 16% in DR than that of AL. Median and maximal lifespans significantly increased (28.5% and 16.4%, respectively) by DR, and also lowered superoxide radical about 15~45% in DR compared with AL at 4, 8 and 12 months of age. On the other hand, superoxide dismutase (SOD) activities were higher (about 15~30%) in DR than those in AL group of SAMP8 except for 4 months of age. Our results suggest that 40% calorie restricted SAMP8 can effectively suppress dementia-related abnormalities during aging.






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