(-)-Gallocatechin gallate from green tea rescues cognitive impairment through restoring hippocampal silent synapses in post-menopausal depression.

Post-menopausal depression (PMD) is a common psychological disorder accompanied by a cognitive deficit, which is caused by a series of uncontrolled emotional disruptions by strong environmental stressors during menopause. To overcome PMD-induced cognitive deficit, Green tea has been suggested as a dietary supplement because of its ameliorating effect on cognitive dysfunction induced by normal aging or neurodegenerative syndromes; however, its clinical use to improve PMD-accompanied cognitive deficit is still limited due to the controversy for the active ingredients and ambiguous mechanism of its action. Here, we developed modified high-temperature-processed green tea extract (HTP-GTE), which showed lower neuronal toxicity than the conventional green tea extract (GTE). We also demonstrated that HTP-GTE administration prevented the development of learned helplessness (LH) in a rat post-menopausal model. Additionally, HTP-GTE improved LH-induced cognitive impairments simultaneously with rescued the long-term synaptic plasticity. This occurred via the restoration of silent synapse formation by increasing the hippocampal BDNF-tyrosine receptor kinase B pathway in the helpless ovariectomized (OVX) rats. Likewise, we also identified that (-)-gallocatechin gallate was the main contributor of the HTP-GTE effect. Our findings suggested that HTP-GTE has a potential as a preventive nutritional supplement to ameliorate cognitive dysfunctions associated with PMD.

Rapeseed oil fortified with micronutrients improves cognitive alterations associated with metabolic syndrome.

Metabolic syndrome represents a major risk factor for severe comorbidities such as cardiovascular diseases or diabetes. It is also associated with an increased prevalence of emotional and cognitive alterations that in turn aggravate the disease and related outcomes. Identifying therapeutic strategies able to improve those alterations is therefore a major socioeconomical and public health challenge. We previously reported that both hippocampal inflammatory processes and neuronal plasticity contribute to the development of emotional and cognitive alterations in db/db mice, an experimental model of metabolic syndrome that displays most of the classical features of the syndrome. In that context, nutritional interventions with known impact on those neurobiological processes appear as a promising alternative to limit the development of neurobiological comorbidities of metabolic syndrome. We therefore tested here whether n-3 polyunsaturated fatty acids (n-3 PUFAs) associated with a cocktail of antioxidants can protect against the development of behavioral alterations that accompany the metabolic syndrome. Thus, this study aimed: 1) to evaluate if a diet supplemented with the plant-derived n-3 PUFA α-linolenic acid (ALA) and antioxidants (provided by n-3 PUFAs-rich rapeseed oil fortified with a mix of naturally constituting antioxidant micronutrients, including coenzyme Q10, tocopherol, and the phenolic compound canolol) improved behavioral alterations in db/db mice, and 2) to decipher the biological mechanisms underlying this behavioral effect. Although the supplemented diet did not improve anxiety-like behavior and inflammatory abnormalities, it reversed hippocampus-dependent spatial memory deficits displayed by db/db mice in a water maze task. It concomitantly changed subunit composition of glutamatergic AMPA and NMDA receptors in the hippocampus that has been shown to modulate synaptic function related to spatial memory. These data suggest that changes in local neuronal plasticity may underlie cognitive improvements in db/db mice fed the supplemented diet. The current findings might therefore provide valuable data for introducing new nutritional strategies for the treatment of behavioral complications associated with MetS.

Choline Supplementation Ameliorates Behavioral Deficits and Alzheimer's Disease-Like Pathology in Transgenic APP/PS1 Mice.

SCOPE: Alzheimer's disease (AD) is a detrimental neurodegenerative disease and has no known effective treatment. The essential nutrient choline potentially plays an important role in cognition. Perinatal choline supplementation (CS) is critical for memory performance. Findings have shown that postnatal choline-containing compounds enhance memory functions in populations with memory impairments. However, whether CS can be targeted to decelerate the progression of AD remains unknown. METHODS AND RESULTS: APP/PS1 mice and their wild-type littermates are fed either a control or CS diet from 2 to 11 months of age. As compared to WT mice, APP/PS1 mice on the control diet are characterized by the reduction in the number of cholinergic neurons in the basal forebrain, reduced cholinergic fiber staining intensity in the amygdala, and reduced hippocampal and cerebral cortical levels of choline and acetylcholine. CS partially prevents these changes and ameliorates cognitive deficits and anxiety. Furthermore, amyloid-ß deposition and microgliosis are decreased in the APP/PS1 mice fed a CS diet. These effects may have been due to inhibition of NLRP3 inflammasome activation and restoration of synapse membrane formation. CONCLUSION: These findings reveal a beneficial effect of CS on AD progression during adulthood and provide a likely therapeutic intervention for AD patients.

Nutrition and Chronic Conditions.

This editorial discusses and analyses the role of dietary interventions in the management of chronic conditions in recognition of the global increase of these diseases, the rise in the ageing population, and the significant cost to health services around the world. Evidence has shown that low-glycaemic index (GI) and low-carbohydrate diets are effective in the management of type 2 diabetes, and the role of unsaturated fatty acids, vitamins, and bioactive compounds in chronic disease management have been the subject of intense research. However, although multidimensional approaches are important in the management of these chronic conditions, nutritional interventions are critical and central to these strategies.

Cerebrosides from Sea Cucumber Improved Aß1-42 -Induced Cognitive Deficiency in a Rat Model of Alzheimer's Disease.

SCOPE: Cerebrosides are a class of neutral glycosphingolipids, which are widely found to be present in brain tissue. In this study, the protective effect of sea cucumber cerebrosides (Cer) against ß-amyloid (Aß)-induced cognitive impairment is investigated. METHODS AND RESULTS: Male SD rats receive a ventricle injection Aß1-42 peptide to establish an Alzheimer's disease model. Then, the protective effects of Cer against Aß1-42 -induced cognitive impairment by gavage and feed addition are evaluated. The Morris water maze test results show that oral administration of Cer can significantly ameliorate Aß1-42 -induced cognitive deficiency at both high dose (200 mg per kg·per day) and low dose (40 mg per kg·per day) for 27 days. Dietary supplement of Cer by feed addition also exhibits the amelioration on the impaired cognitive function. Further findings indicate that Cer ameliorates Aß1-42 -induced neuronal damage and suppresses the induced apoptosis by decreasing the level of Bax/Bcl-2. Additionally, Cer enhances the expressions of PSD-95 and synaptophysin by activating BDNF/TrkB/CREB signaling pathway, thereby ameliorating Aß1-42 -induced synaptic dysfunction. Furthermore, Cer attenuates Aß1-42 -induced tau hyperphosphorylation by activating the PI3K/Akt/GSK3ß signaling pathway. CONCLUSION: Sea cucumber cerebrosides possess neuroprotective effects against Aß1-42 -triggered cognitive deficits, which may be a potential nutritional preventive strategy for neurodegenerative diseases.

Nutritional interventions and cognitive-related outcomes in patients with late-life cognitive disorders: A systematic review.

There have been a large number of observational studies on the impact of nutrition on neuroprotection, however, there was a lack of evidence from randomized clinical trials (RCTs). In the present systematic review, from the 32 included RCTs published in the last four years (2014-2017) in patients aged 60 years and older with different late-life cognitive disorders, nutritional intervention through medical food/nutraceutical supplementation and multidomain approach improved magnetic resonance imaging findings and other cognitive-related biomarkers, but without clear effect on cognition in mild Alzheimer's disease (AD) and mild cognitive impairment (MCI). Antioxidant-rich foods (nuts, grapes, cherries) and fatty acid supplementation, mainly n-3 polyunsaturated fatty acids (PUFA), improved specific cognitive domains and cognitive-related outcomes in MCI, mild-to-moderate dementia, and AD. Antioxidant vitamin and trace element supplementations improved only cognitive-related outcomes and biomarkers, high-dose B vitamin supplementation in AD and MCI patients improved cognitive outcomes in the subjects with a high baseline plasma n-3 PUFA, while folic acid supplementation had positive impact on specific cognitive domains in those with high homocysteine.

[Nutrition strategies that improve cognitive function]. / Estrategias nutricionales que mejoran la función cognitiva.

Cognitive capacity can be influenced by components of the diet. Low glycemic index foods seem to improve attention, memory and functional capacity, while those rich in simple sugars are associated with difficulty in concentration and attention. The brain needs a continuous supply of amino acids for the synthesis of neurotransmitters, especially serotonin and catecholamines. Low levels of serotonin have been linked to decreased learning, reasoning and memory. The quality and type of dietary fat can also affect intellectual and mental capacity. High saturated fat intake has been related to cognitive deterioration while the consumption of polyunsaturated fatty acids (docosahexaenoic acid) has beneficial effects in their prevention. It is advisable to consume diets with an adequate ratio (5:1) of omega-6: 3 fatty acids (Mediterranean diet) given that they are associated with better memory capacity and lower risk of cognitive deterioration. Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects and improve intellectual performance. In parallel, antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin) have a very important role in the defense against oxidative stress associated with mental deterioration and in the improvement of cognition. Currently, there is a high consumption of diets rich in saturated fats and refined sugars and low intake of fruits, vegetables and water that can negatively affect cognitive ability. Adequate nutrition is necessary to optimize brain function and prevent cognitive decline.

La capacidad cognitiva puede verse influida por los componentes de la dieta. Los alimentos de bajo índice glucémico parecen mejorar la atención, la memoria y la capacidad funcional, mientras que los ricos en azúcares simples se asocian con dificultad de concentración y atención.El cerebro necesita un aporte continuado de aminoácidos para la síntesis de neurotransmisores, especialmente serotonina y catecolaminas. Niveles bajos de serotonina se han relacionado con una disminución del aprendizaje, del razonamiento y de la memoria.La calidad y el tipo de grasa alimentaria también pueden afectar a la función intelectual y mental. La elevada ingesta de grasa saturada se ha relacionado con un deterioro cognitivo, mientras que el consumo de ácidos grasos poliinsaturados (docosahexaenoico) tiene efectos beneficiosos en su prevención. Es aconsejable el consumo de dietas con una adecuada proporción (5:1) de ácidos grasos omega-6:3 (dieta mediterránea), dado que se asocian con una mejor memoria y un menor riesgo de deterioro cognitivo.Las vitaminas B1, B6, B12, B9 (ácido fólico) y D, colina, hierro y yodo ejercen efectos neuroprotectores y mejoran el rendimiento intelectual. Paralelamente, los antioxidantes (vitaminas C, E y A, cinc, selenio, luteína y zeaxantina) tienen un papel muy importante en la defensa contra el estrés oxidativo asociado al deterioro mental y en la mejora de la cognición.Actualmente, existe un elevado consumo de dietas ricas en grasas saturadas y azúcares refinados y baja ingesta de frutas, verduras y agua, lo que puede ser desfavorable para la capacidad cognitiva.Una nutrición adecuada es necesaria para optimizar la función cerebral y prevenir el deterioro cognitivo.

Estrategias nutricionales que mejoran la función cognitiva / Nutrition strategies that improve cognitive function

La capacidad cognitiva puede verse influida por los componentes de la dieta. Los alimentos de bajo índice glucémico parecen mejorar la atención, la memoria y la capacidad funcional, mientras que los ricos en azúcares simples se asocian con dificultad de concentración y atención. El cerebro necesita un aporte continuado de aminoácidos para la síntesis de neurotransmisores, especialmente serotonina y catecolaminas. Niveles bajos de serotonina se han relacionado con una disminución del aprendizaje, del razonamiento y de la memoria. La calidad y el tipo de grasa alimentaria también pueden afectar a la función intelectual y mental. La elevada ingesta de grasa saturada se ha relacionado con un deterioro cognitivo, mientras que el consumo de ácidos grasos poliinsaturados (docosahexaenoico) tiene efectos beneficiosos en su prevención. Es aconsejable el consumo de dietas con una adecuada proporción (5:1) de ácidos grasos omega-6:3 (dieta mediterránea), dado que se asocian con una mejor memoria y un menor riesgo de deterioro cognitivo. Las vitaminas B1, B6, B12, B9 (ácido fólico) y D, colina, hierro y yodo ejercen efectos neuroprotectores y mejoran el rendimiento intelectual. Paralelamente, los antioxidantes (vitaminas C, E y A, cinc, selenio, luteína y zeaxantina) tienen un papel muy importante en la defensa contra el estrés oxidativo asociado al deterioro mental y en la mejora de la cognición. Actualmente, existe un elevado consumo de dietas ricas en grasas saturadas y azúcares refinados y baja ingesta de frutas, verduras y agua, lo que puede ser desfavorable para la capacidad cognitiva. Una nutrición adecuada es necesaria para optimizar la función cerebral y prevenir el deterioro cognitivo

Cognitive capacity can be influenced by components of the diet. Low glycemic index foods seem to improve attention, memory and functional capacity, while those rich in simple sugars are associated with difficulty in concentration and attention. The brain needs a continuous supply of amino acids for the synthesis of neurotransmitters, especially serotonin and catecholamines. Low levels of serotonin have been linked to decreased learning, reasoning and memory. The quality and type of dietary fat can also affect intellectual and mental capacity. High saturated fat intake has been related to cognitive deterioration while the consumption of polyunsaturated fatty acids (docosahexaenoic acid) has beneficial effects in their prevention. It is advisable to consume diets with an adequate ratio (5:1) of omega-6: 3 fatty acids (Mediterranean diet) given that they are associated with better memory capacity and lower risk of cognitive deterioration. Vitamins B1, B6, B12, B9 (folic acid) and D, choline, iron and iodine exert neuroprotective effects and improve intellectual performance. In parallel, antioxidants (vitamins C, E, A, zinc, selenium, lutein and zeaxanthin) have a very important role in the defense against oxidative stress associated with mental deterioration and in the improvement of cognition. Currently, there is a high consumption of diets rich in saturated fats and refined sugars and low intake of fruits, vegetables and water that can negatively affect cognitive ability. Adequate nutrition is necessary to optimize brain function and prevent cognitive decline

The Role of Nutrition in Cognitive Function and Brain Ageing in the Elderly.

PURPOSE OF REVIEW: The purposes of this review were to examine literature published over the last 5 years and to evaluate the role of nutrition in cognitive function and brain ageing, focussing on the Mediterranean diet (MeDi), Dietary Approaches to Stop Hypertension (DASH), and Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diets. RECENT FINDINGS: Results suggest that higher adherence to a healthy dietary pattern is associated with preservation of brain structure and function as well as slower cognitive decline, with the MIND diet substantially slowing cognitive decline, over and above the MeDi and DASH diets. Whilst results to-date suggest adherence to a healthy diet, such as the MeDi, DASH, or MIND, is an important modifiable risk factor in the quest to develop strategies aimed at increasing likelihood of healthy brain ageing, further work is required to develop dietary guidelines with the greatest potential benefit for public health; a research topic of increasing importance as the world's population ages.

Mediterranean Diet in Preventing Neurodegenerative Diseases.

PURPOSE OF REVIEW: We reviewed the most recent literature examining the associations between the Mediterranean-style diet (MD), neurodegenerative diseases, and markers and mechanisms of neurodegeneration. RECENT FINDINGS: Most, but not all, epidemiologic studies report a protective association between MD adherence, cognitive impairment, and brain health. Data from clinical trials supporting these observational findings are also emerging. Limited evidence suggests that MD adherence may be protective for Parkinson's disease risk. Mechanistically, plant polyphenols may activate similar molecular pathways as caloric restriction diets, which helps explain the neuroprotective properties of the MD. Evidence for cognitive disorders is abundant, but there is a dearth of literature for other neurodegenerative disorders and for markers of neurodegeneration. Further research is needed to elucidate the protective role of MD on neurodegeneration, the most salient components of the MD, and the most sensitive time periods over the lifecourse at which the MD may exert its effects.

Effects of 2-day calorie restriction on cardiovascular autonomic response, mood, and cognitive and motor functions in obese young adult women.

Although long-term energy restriction has been widely investigated and has consistently induced improvements in health and cognitive and motor functions, the responses to short-duration calorie restriction are not completely understood. The purpose of this study was to investigate the effects of a 2-day very low-calorie diet on evoked stress, mood, and cognitive and motor functions in obese women. Nine obese women (body fatness > 32%) aged 22-31 years were tested under two randomly allocated conditions: 2-day very low-calorie diet (511 kcal) and 2-day usual diet. The perceived stressfulness of the diet, cardiovascular autonomic response, and cognitive and motor performances were evaluated before and after each diet. The subjective stress rating of the calorie-restricted diet was 41.5 ± 23.3. Calorie restriction had no detectable effects on the heart rate variability indices, mood, grip strength, or psychomotor functions. By contrast, calorie restriction increased (p < 0.05) spatial processing and visuospatial working memory accuracy, and decreased (p < 0.05) accuracy of cognitive flexibility. In conclusion, our results demonstrate that although a 2-day calorie restriction evoked moderate stress in obese women, cardiovascular autonomic function was not affected. Calorie restriction had complex effects on cognition: it declined cognitive flexibility, and improved spatial processing and visuospatial working memory, but did not affect mood or motor behavior.

Nutritional Intervention as a Preventive Approach for Cognitive-Related Outcomes in Cognitively Healthy Older Adults: A Systematic Review.

The link diet-cognitive function/dementia has been largely investigated in observational studies; however, there was a lack of evidence from randomized clinical trials (RCTs) on the prevention of late-life cognitive disorders though dietary intervention in cognitively healthy older adults. In the present article, we systematically reviewed RCTs published in the last four years (2014-2017) exploring nutritional intervention efficacy in preventing the onset of late-life cognitive disorders and dementia in cognitively healthy subjects aged 60 years and older using different levels of investigation (i.e., dietary pattern changes/medical food/nutraceutical supplementation/multidomain approach and dietary macro- and micronutrient approaches) as well as possible underlying mechanisms of nutritional prevention. From the 35 included RCTs, there was moderate evidence that intervention through dietary pattern changes, medical food/nutraceutical supplementation, and multidomain approach improved specific cognitive domains or cognitive-related blood biomarkers. There was high evidence that protein supplementation improved specific cognitive domains or functional status in prefrail older adults without effect on cognitive function. For fatty acid supplementation, mainly long-chain polyunsaturated fatty acids, there was emerging evidence suggesting an impact of this approach in improving specific cognitive domains, magnetic resonance imaging (MRI) findings, and/or cognitive-related biomarkers also in selected subgroups of older subjects, although some results were conflicting. There was convincing evidence of an impact of non-flavonoid polyphenol and flavonoid supplementations in improving specific cognitive domains and/or MRI findings. Finally, there was only low evidence suggesting efficacy of intervention with homocysteine-related and antioxidant vitamins in improving cognitive functions, dementia incidence, or cognitive-related biomarkers in cognitively healthy older subjects.

Diet Supplementation with Hydroxytyrosol Ameliorates Brain Pathology and Restores Cognitive Functions in a Mouse Model of Amyloid-ß Deposition.

Alzheimer's disease is the most common form of dementia affecting a large proportion of aged people. Plant polyphenols have been reported to be potentially useful in the prevention of AD due to their multiple pharmacological activities. The aim of the present study was to assess whether the previously reported neuroprotective and anti-inflammatory effects resulting from oleuropein aglycone administration were reproduced by diet supplementation with similar amounts of its metabolite hydoxytyrosol (HT). Four-month-old TgCRND8 and wild type mice were treated for 8 weeks with a low-fat diet (5%) supplemented with HT (50 mg/kg of diet). We found that HT supplementation significantly improved cognitive functions of TgCRND8 mice and significantly reduced Aß42 and pE3-Aß plaque area and number in the cortex; in the hippocampal areas of HT-fed TgCRND8 mice, we found a significant reduction in the pE3-Aß plaque number together with a tendency toward a reduction in Aß42 load and pE3-Aß plaque area, associated with a marked reduction of TNF-α expression and astrocyte reaction. Macroautophagy induction and modulation of MAPKs signaling were found to underlie the beneficial effects of HT. Our findings indicate that HT administration reproduces substantially the beneficial effects on behavioral performance and neuropathology previously reported in TgCRND8 mice fed with oleuropein aglycone, resulting in comparable neuroprotection.

A Study of a Supplement Containing Huperzine A and Curcumin in Dementia Patients and Individuals with Mild Cognitive Impairment.

Extracts from Huperzia serrata (HS) function as a cholinesterase inhibitor and a glutamic acid receptor antagonist. We tested a supplement containing HS extracts, curcumin, and others in dementia patients and individuals with mild cognitive impairment (MCI) in an open label study. Most patients with Alzheimer's disease, dementia with Lewy bodies, and MCI individuals exhibited improvements in cognitive functions, as assessed by the Alzheimer's Disease Assessment Scale-cognitive subscale Japanese version. The scores were significantly improved at 6-12 weeks compared with baseline scores (p = 0.007) and at 22-28 weeks (p = 0.004). Thus, this supplement may be administered to dementia patients as well as MCI individuals.

[Epilepsy, cognition and ketogenic diet]. / Epilepsia, cognicion y dieta cetogenica.

INTRODUCTION: Most individuals with epilepsy will respond to pharmacologic treatment; however, approximately 20-30% will develop medically refractory epilepsy. Cognitive side effects of antiepileptic drugs are common and can negatively affect tolerability, compliance, and long-term retention of the treatment. Ketogenic diet is an effective and well-tolerated treatment for these children with refractory epilepsy without any negative effect on cognition or behavior. AIM: To review the current state of experimental and clinical data concerning the neuroprotective and cognitive effects of the ketogenic diet in both humans and animals. DEVELOPMENT: In different animal models, with or without epilepsy, the ketogenic diet seems to have neuroprotective and mood-stabilizing effects. In the observational studies in pediatric epilepsy, improvements during treatment with the ketogenic diet are reported in behavior and cognitive function, particularly with respect to attention, alertness, activity level, socialization, and sleep quality. One randomized controlled trial in patients with pediatric refractory epilepsy showed a mood and cognitive activation during ketogenic diet treatment. CONCLUSIONS: Ketogenic diet shows a positive impact on behavioral and cognitive functioning in children and adolescents with refractory epilepsy. More specifically, an improvement is observed in mood, sustained attention, and social interaction.

TITLE: Epilepsia, cognicion y dieta cetogenica.Introduccion. Aunque generalmente se controlan bien con medicacion, hasta un 20-30% de las epilepsias infantiles son refractarias al tratamiento farmacologico. Los efectos adversos cognitivos de los farmacos antiepilepticos son frecuentes y pueden afectar negativamente la tolerabilidad, el cumplimiento y el mantenimiento a largo plazo del tratamiento antiepileptico. La dieta cetogenica es un tratamiento eficaz y bien tolerado para las epilepsias infantiles refractarias y no muestra efectos adversos negativos sobre cognicion o conducta. Objetivo. Revisar la evidencia actual existente con respecto a los estudios experimentales y clinicos que analizan los efectos neuroprotectores y cognitivos de la dieta cetogenica, tanto en humanos como en animales de experimentacion. Desarrollo. La dieta cetogenica muestra efectos neuroprotectores y estabilizadores del estado de animo en diversos modelos animales, con o sin epilepsia. En los estudios observacionales en epilepsia infantil se refieren mejorias en cognicion y conducta durante el tratamiento con dieta cetogenica, especialmente evidentes en atencion, nivel de alerta y actividad, socializacion y calidad del sueño. En un estudio aleatorizado controlado en pacientes con epilepsia infantil refractaria, la dieta cetogenica mostro una activacion evolutiva evidente sobre la cognicion y el estado de animo. Conclusiones. La dieta cetogenica tiene un impacto positivo sobre el funcionamiento conductual y cognitivo en niños y adolescentes con epilepsia refractaria. Esta mejoria es mas evidente con respecto a estado de animo, atencion sostenida e interaccion social.

Epilepsia, cognición y dieta cetogénica / Epilepsy, cognition and ketogenic diet

Introducción. Aunque generalmente se controlan bien con medicación, hasta un 20-30% de las epilepsias infantiles son refractarias al tratamiento farmacológico. Los efectos adversos cognitivos de los fármacos antiepilépticos son frecuentes y pueden afectar negativamente la tolerabilidad, el cumplimiento y el mantenimiento a largo plazo del tratamiento antiepiléptico. La dieta cetogénica es un tratamiento eficaz y bien tolerado para las epilepsias infantiles refractarias y no muestra efectos adversos negativos sobre cognición o conducta. Objetivo. Revisar la evidencia actual existente con respecto a los estudios experimentales y clínicos que analizan los efectos neuroprotectores y cognitivos de la dieta cetogénica, tanto en humanos como en animales de experimentación. Desarrollo. La dieta cetogénica muestra efectos neuroprotectores y estabilizadores del estado de ánimo en diversos modelos animales, con o sin epilepsia. En los estudios observacionales en epilepsia infantil se refieren mejorías en cognición y conducta durante el tratamiento con dieta cetogénica, especialmente evidentes en atención, nivel de alerta y actividad, socialización y calidad del sueño. En un estudio aleatorizado controlado en pacientes con epilepsia infantil refractaria, la dieta cetogénica mostró una activación evolutiva evidente sobre la cognición y el estado de ánimo. Conclusiones. La dieta cetogénica tiene un impacto positivo sobre el funcionamiento conductual y cognitivo en niños y adolescentes con epilepsia refractaria. Esta mejoría es más evidente con respecto a estado de ánimo, atención sostenida e interacción social (AU)

Introduction. Most individuals with epilepsy will respond to pharmacologic treatment; however, approximately 20-30% will develop medically refractory epilepsy. Cognitive side effects of antiepileptic drugs are common and can negatively affect tolerability, compliance, and long-term retention of the treatment. Ketogenic diet is an effective and well-tolerated treatment for these children with refractory epilepsy without any negative effect on cognition or behavior. Aim. To review the current state of experimental and clinical data concerning the neuroprotective and cognitive effects of the ketogenic diet in both humans and animals. Development. In different animal models, with or without epilepsy, the ketogenic diet seems to have neuroprotective and mood-stabilizing effects. In the observational studies in pediatric epilepsy, improvements during treatment with the ketogenic diet are reported in behavior and cognitive function, particularly with respect to attention, alertness, activity level, socialization, and sleep quality. One randomized controlled trial in patients with pediatric refractory epilepsy showed a mood and cognitive activation during ketogenic diet treatment. Conclusions. Ketogenic diet shows a positive impact on behavioral and cognitive functioning in children and adolescents with refractory epilepsy. More specifically, an improvement is observed in mood, sustained attention, and social interaction (AU)

Potential for diet to prevent and remediate cognitive deficits in neurological disorders.

The pathophysiology of many neurological disorders involves oxidative stress, neuroinflammation, and mitochondrial dysfunction. There is now substantial evidence that diet can decrease these forms of pathophysiology, and an emerging body of literature relatedly suggests that diet can also prevent or even remediate the cognitive deficits observed in neurological disorders that exhibit such pathology (eg, Alzheimer's disease, multiple sclerosis, age-related cognitive decline, epilepsy). The current review summarizes the emerging evidence in relation to whole diets prominent in the scientific literature-ketogenic, caloric restriction, high polyphenol, and Mediterranean diets-and provides a discussion of the possible underlying neurophysiological mechanisms.

Poor cognitive ageing: Vulnerabilities, mechanisms and the impact of nutritional interventions.

BACKGROUND: Ageing is a highly complex process marked by a temporal cascade of events, which promote alterations in the normal functioning of an individual organism. The triggers of normal brain ageing are not well understood, even less so the factors which initiate and steer the neuronal degeneration, which underpin disorders such as dementia. A wealth of data on how nutrients and diets may support cognitive function and preserve brain health are available, yet the molecular mechanisms underlying their biological action in both normal ageing, age-related cognitive decline, and in the development of neurodegenerative disorders have not been clearly elucidated. OBJECTIVES: This review aims to summarise the current state of knowledge of vulnerabilities that predispose towards dysfunctional brain ageing, highlight potential protective mechanisms, and discuss dietary interventions that may be used as therapies. A special focus of this paper is on the impact of nutrition on neuroprotection and the underlying molecular mechanisms, and this focus reflects the discussions held during the 2nd workshop 'Nutrition for the Ageing Brain: Functional Aspects and Mechanisms' in Copenhagen in June 2016. The present review is the most recent in a series produced by the Nutrition and Mental Performance Task Force under the auspice of the International Life Sciences Institute Europe (ILSI Europe). CONCLUSION: Coupling studies of cognitive ageing with studies investigating the effect of nutrition and dietary interventions as strategies targeting specific mechanisms, such as neurogenesis, protein clearance, inflammation, and non-coding and microRNAs is of high value. Future research on the impact of nutrition on cognitive ageing will need to adopt a longitudinal approach and multimodal nutritional interventions will likely need to be imposed in early-life to observe significant impact in older age.

Intake of Fruit and Vegetables and the Incident Risk of Cognitive Disorders: A Systematic Review and Meta-Analysis of Cohort Studies.

OBJECTIVES: No quantitative assessment has been performed to specifically link the consumption of fruit and vegetables with the incident risk of cognitive disorders. METHODS: We searched the PubMed and the Embase databases (both from the inception to June 13th, 2016) for records that report the intake of fruit and vegetables and the risk of developing cognitive disorders (Alzheimer's disease, dementia, and cognitive decline/impairment). A generic inverse-variance method (random-effects model) was used to combine the relative risks (RRs) and 95% confidence intervals (CIs). To explore the potential sources of heterogeneity, we performed the subgroup and meta-regression analyses by pre-specified characteristics. RESULTS: We identified 6 cohorts involving a total of 21,175 participants. The pooled analysis showed that consumption of fruit and vegetables was inversely associated with the incident risk of cognitive disorders, and the pooled RR (95% CI) was 0.74 (0.62, 0.88), with evidence of significant heterogeneity (I2 =68%). Furthermore, we found that the significant heterogeneity might be attributed to the ethnic difference. CONCLUSION: Further large prospective studies should be performed to quantify the potential dose-response patterns of fruit and/or vegetables intake and to explore the role of fruit or vegetables consumption separately on cognitive disorders in different populations.