ABSTRACT
Oxidative stress plays a fundamental role in the pathogenesis of Parkinson's disease (PD). Oxidative stress appears to be responsible for the gradual dysfunction that manifests via numerous cellular pathways throughout PD progression. This review will describe the prooxidant effect of excessive consumption of processed food. Processed meat can affect health due to its high sodium content, advanced lipid oxidation end-products, cholesterol, and free fatty acids. During cooking, lipids can react with proteins to form advanced end-products of lipid oxidation. Excessive consumption of different types of carbohydrates is a risk factor for PD. The antioxidant effects of some foods in the regular diet provide an inconclusive interpretation of the environment's mechanisms with the modulation of oxidation stress-induced PD. Some antioxidant molecules are known whose primary mechanism is the neuroprotective effect. The melatonin mechanism consists of neutralizing reactive oxygen species (ROS) and inducing antioxidant enzyme's expression and activity. N-acetylcysteine protects against the development of PD by restoring levels of brain glutathione. The balanced administration of vitamin B3, ascorbic acid, vitamin D and the intake of caffeine every day seem beneficial for brain health in PD. Excessive chocolate intake could have adverse effects in PD patients. The findings reported to date do not provide clear benefits for a possible efficient therapeutic intervention by consuming the nutrients that are consumed regularly.
Subject(s)
Antioxidants/therapeutic use , Food Microbiology/methods , Parkinson Disease/diet therapy , Reactive Oxygen Species/adverse effects , Antioxidants/pharmacology , Diet , HumansABSTRACT
Evidence suggests that idiopathic Parkinson's disease (PD) is the consequence of a neurodevelopmental disruption, rather than strictly a consequence of aging. Thus, we hypothesized that maternal supplement of omega-3 polyunsaturated fatty acids (ω-3 PUFA) may be associated with neuroprotection mechanisms in a self-sustaining cycle of neuroinflammation and neurodegeneration in lipopolysaccharide (LPS)-model of PD. To test this hypothesis, behavioral and neurochemical assay were performed in prenatally LPS-exposed offspring at postnatal day 21. To further determine whether prenatal LPS exposure and maternal ω-3 PUFAs supplementation had persisting effects, brain injury was induced on PN 90 rats, following bilateral intranigral LPS injection. Pre- and postnatal inflammation damage not only affected dopaminergic neurons directly, but it also modified critical features, such as activated microglia and astrocyte cells, disrupting the support provided by the microenvironment. Unexpectedly, our results failed to show any involvement of caspase-dependent and independent apoptosis pathway in neuronal death mechanisms. On the other hand, learning and memory deficits detected with a second toxic exposure were significantly attenuated in maternal ω-3 PUFAs supplementation group. In addition, ω-3 PUFAs promote beneficial effect on synaptic function, maintaining the neurochemical integrity in remaining neurons, without necessarily protect them from neuronal death. Thus, our results suggest that ω-3 PUFAs affect the functional ability of the central nervous system in a complex way in a multiple inflammation-induced neurotoxicity animal model of PD and they disclose new ways of understanding how these fatty acids control responses of the brain to different challenges.
Subject(s)
Disease Models, Animal , Dopaminergic Neurons/metabolism , Fatty Acids, Omega-3/administration & dosage , Parkinson Disease/diet therapy , Parkinson Disease/metabolism , Prenatal Nutritional Physiological Phenomena/physiology , Animals , Animals, Newborn , Dietary Supplements , Dopaminergic Neurons/drug effects , Dopaminergic Neurons/pathology , Female , Inflammation/diet therapy , Inflammation/metabolism , Inflammation/pathology , Male , Neuroprotective Agents/administration & dosage , Parkinson Disease/pathology , Pregnancy , Prenatal Nutritional Physiological Phenomena/drug effects , Random Allocation , Rats , Rats, WistarABSTRACT
The brain has a central role in the regulation of energy stability of the organism. It is the organ with the highest energetic demands, the most susceptible to energy deficits, and is responsible for coordinating behavioral and physiological responses related to food foraging and intake. Dietary interventions have been shown to be a very effective means to extend lifespan and delay the appearance of age-related pathological conditions, notably those associated with brain functional decline. The present review focuses on the effects of these interventions on brain metabolism and cerebral redox state, and summarizes the current literature dealing with dietary interventions on brain pathology.
Subject(s)
Brain/metabolism , Caloric Restriction , Energy Metabolism , Aging , Alzheimer Disease/diet therapy , Amyotrophic Lateral Sclerosis/diet therapy , Animals , Arcuate Nucleus of Hypothalamus/physiology , Autophagy , Dietary Supplements , Epilepsy/diet therapy , Fatty Acids/metabolism , Feeding Behavior/physiology , Humans , Insulin Resistance , Longevity , Mitochondria/metabolism , Models, Biological , Nucleus Accumbens/physiology , Oxidation-Reduction , Paraventricular Hypothalamic Nucleus/physiology , Parkinson Disease/diet therapy , Signal Transduction , Sirtuin 1/physiology , Stroke/diet therapyABSTRACT
Parkinson's disease (PD) is a neurodegenerative disorder characterized by decreased dopamine, intracellular inclusions (Lewy bodies) and brain iron deposits. PD has also been related with reduced ferroxidase activity, diminished antioxidant defenses and lipid peroxidation. Striatal injection of 1-methyl-4-phenylpyridinium (MPP(+)) into rodents reproduces the major biochemical characteristics of PD, including oxidative stress. Copper (Cu) plays an important role as prosthetic group of several proteins involved in iron metabolism and antioxidant responses, such as ceruloplasmin (Cp). In the present study, intraperitoneal CuSO4 injection (10µmol/kg) produced an insignificant increase of Cu content in striatum and midbrain (17.5% and 7%, respectively). After 10 and 11h, Cu induced 6- and 4-fold increase Cp mRNA in midbrain and striatum, respectively. Cu-supplement also produced a time-dependent increase ferroxidase activity in striatal tissue, reaching a maximum 16h after Cu treatment in midbrain; while, ferrous iron content diminished 18% in striatum and 8% in midbrain. In regard the PD model, we found that MPP(+) (10µg/8µL, intrastriatal), induced a significant (P<0.05) reduction of striatal ferroxidase activity; this effect was reverted by Cu pre-treatment 16h before MPP(+). Likewise, Cu-supplement prevented lipid fluorescent products formation in striatum, evaluated (P<0.01) 6h after MPP(+). In the long term, apomorphine-evoked circling behavior was evaluated 6 days after MPP(+) injury; Cu pre-treatment significantly reduced (P<0.05) the apomorphine-induced ipsilateral turns in MPP(+)-lesioned rats. These results suggest that Cu-induced expression of Cp could be an interesting scope against the deleterious effects of iron deposits in PD.
Subject(s)
1-Methyl-4-phenylpyridinium/metabolism , Ceruloplasmin/metabolism , Copper/pharmacology , Corpus Striatum/metabolism , 1-Methyl-4-phenylpyridinium/pharmacology , 1-Methyl-4-phenylpyridinium/toxicity , Animals , Copper/pharmacokinetics , Copper Sulfate/administration & dosage , Copper Sulfate/pharmacology , Corpus Striatum/drug effects , Disease Models, Animal , Male , Mesencephalon/drug effects , Mesencephalon/metabolism , Parkinson Disease/diet therapy , Parkinson Disease/prevention & control , Rats , Rats, WistarABSTRACT
Ginkgo Biloba extract 761 (EGb 761) is a patented and well-defined mixture of active compounds extracted from Ginkgo biloba leaves. This extract contains two main groups of active compounds, flavonoids (24%) and terpenoids (6%). EGb 761 is used clinically to treat dementia and vaso-occlusive and cochleovestibular disorders. This extract has neuroprotective effects, exerted probably by means of its antioxidant function. Parkinson's disease (PD) is a neurodegenerative disorder that affects 2% of the population older than 60 y. It produces a progressive loss of dopaminergic neurons and depletion of dopamine (DA), leading to movement impairment. The production of reactive oxygen species, which act as mediators of oxidative damage, is linked to PD. This disease is routinely treated with the DA precursor, L-3,4-dihydroxyphenylalanine. However, this produces severe side effects, and its neurotoxic properties can be due to a free radical production. Thus, administration of antioxidant drugs might be used to prevent neuronal death produced by oxidative mechanisms. The use of synthetic antioxidants has decreased because of their suspected activity as carcinogenic promoters. We describe the studies related to the antioxidant effect of EGb 761 in an animal model of PD. It has been shown that EGb761 can provide a neuroprotective/neurorecovery effect against the damage to midbrain DA neurons in an animal model of PD. EGb 761 also has been found to lessen the impairment of locomotion, correlating with an increase of DA and other morphologic and biochemical parameters related to its antioxidant effect in an animal model of PD. These studies suggest it as an alternative in the future treatment of PD.
Subject(s)
Antiparkinson Agents/therapeutic use , Dietary Supplements , Disease Models, Animal , Parkinson Disease/prevention & control , Phytotherapy , Plant Extracts/therapeutic use , Animals , Anti-Inflammatory Agents, Non-Steroidal/adverse effects , Anti-Inflammatory Agents, Non-Steroidal/chemistry , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Antioxidants/adverse effects , Antioxidants/chemistry , Antioxidants/therapeutic use , Antiparkinson Agents/adverse effects , Antiparkinson Agents/chemistry , Apoptosis , Dietary Supplements/adverse effects , Dietary Supplements/analysis , Dopaminergic Neurons/metabolism , Ginkgo biloba , Humans , Mesencephalon/metabolism , Neuroprotective Agents/adverse effects , Neuroprotective Agents/chemistry , Neuroprotective Agents/therapeutic use , Oxidative Stress , Parkinson Disease/diet therapy , Parkinson Disease/metabolism , Plant Extracts/adverse effects , Plant Extracts/chemistryABSTRACT
Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive outpatients with Parkinson's disease (PD), while the classical determinants of homocysteine levels (B6, folic acid, and B12) were usually within normal limits. In contrast, only 3 of 10 consecutive outpatients with dementia without previous stroke had abnormal riboflavin status. The data for 12 patients who did not complete 6 months of therapy or did not comply with the proposed treatment paradigm were excluded from analysis. Nineteen PD patients (8 males and 11 females, mean age +/- SD = 66.2+/-8.6 years; 3, 3, 2, 5, and 6 patients in Hoehn and Yahr stages I to V) received riboflavin orally (30 mg every 8 h) plus their usual symptomatic medications and all red meat was eliminated from their diet. After 1 month the riboflavin status of the patients was normalized from 106.4+/-34.9 to 179.2+/-23 ng/ml (N = 9). Motor capacity was measured by a modification of the scoring system of Hoehn and Yahr, which reports motor capacity as percent. All 19 patients who completed 6 months of treatment showed improved motor capacity during the first three months and most reached a plateau while 5/19 continued to improve in the 3- to 6-month interval. Their average motor capacity increased from 44 to 71% after 6 months, increasing significantly every month compared with their own pretreatment status (P < 0.001, Wilcoxon signed rank test). Discontinuation of riboflavin for several days did not impair motor capacity and yellowish urine was the only side effect observed. The data show that the proposed treatment improves the clinical condition of PD patients. Riboflavin-sensitive mechanisms involved in PD may include glutathione depletion, cumulative mitochondrial DNA mutations, disturbed mitochondrial protein complexes, and abnormal iron metabolism. More studies are required to identify the mechanisms involved.
Subject(s)
Homocysteine/blood , Parkinson Disease/diet therapy , Riboflavin/administration & dosage , Riboflavin/blood , Aged , Female , Humans , Male , Parkinson Disease/blood , Riboflavin Deficiency/blood , Treatment OutcomeABSTRACT
Reportamos un estudio en que se evalúa el uso de dieta rica en fibras (DRF) en el manejo de la constipación en la enfermedad de Parkinson (EP).Se evalúan 14 pacientes con edad media 66.5ñ6.7 años, tiempo de evolución de 7.5ñ5.6. La escala unificada para evaluar EP en su punto III tiene una media de 39.9ñ9.6 puntos. Todos los pacientes presentaban contipación y se les instruyó para consumir DRF (30 gr), fueron evaluados en forma basal y posteriormente al mes. El número de evacuaciones espontáneas antes del uso de DRF fue de 0.5ñ1.0 por semana y al mes de usar DRF 2.2ñ2.0 (p<0.05). Otros parámetros como consistencia de las heces, esfuerzo defecatorio y uso de laxantes presentaron mejprías significativas. La frecuencia de presentación de dolor o disconfort en la defecación y las evacuaciones incompletas no presentaron variaciones de significación