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Diet, Microbiota and Brain Health: Unraveling the Network Intersecting Metabolism and Neurodegeneration.
Gentile, F, Doneddu, PE, Riva, N, Nobile-Orazio, E, Quattrini, A
International journal of molecular sciences. 2020;(20)
Abstract
Increasing evidence gives support for the idea that extra-neuronal factors may affect brain physiology and its predisposition to neurodegenerative diseases. Epidemiological and experimental studies show that nutrition and metabolic disorders such as obesity and type 2 diabetes increase the risk of Alzheimer's and Parkinson's diseases after midlife, while the relationship with amyotrophic lateral sclerosis is uncertain, but suggests a protective effect of features of metabolic syndrome. The microbiota has recently emerged as a novel factor engaging strong interactions with neurons and glia, deeply affecting their function and behavior in these diseases. In particular, recent evidence suggested that gut microbes are involved in the seeding of prion-like proteins and their spreading to the central nervous system. Here, we present a comprehensive review of the impact of metabolism, diet and microbiota in neurodegeneration, by affecting simultaneously several aspects of health regarding energy metabolism, immune system and neuronal function. Advancing technologies may allow researchers in the future to improve investigations in these fields, allowing the buildup of population-based preventive interventions and development of targeted therapeutics to halt progressive neurologic disability.
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2.
Development of the Pediatric Gut Microbiome: Impact on Health and Disease.
Ihekweazu, FD, Versalovic, J
The American journal of the medical sciences. 2018;(5):413-423
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Abstract
The intestinal microbiota are important in human growth and development. Microbial composition may yield insights into the temporal development of microbial communities and vulnerabilities to disorders of microbial ecology such as recurrent Clostridium difficile infection. Discoveries of key microbiome features of carbohydrate and amino acid metabolism are lending new insights into possible therapies or preventative strategies for inflammatory bowel disease (IBD) and irritable bowel syndrome (IBS). In this review, we summarize the current understanding of the development of the pediatric gastrointestinal microbiome, the influence of the microbiome on the developing brain through the gut-brain axis, and the impact of dysbiosis on disease development. Dysbiosis is explored in the context of pediatric allergy and asthma, recurrent C. difficile infection, IBD, IBS, and metabolic disorders. The central premise is that the human intestinal microbiome plays a vital role in health and disease, beginning in the prenatal period and extending throughout childhood.
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Brain-Derived Neurotrophic Factor Expression in Individuals With Schizophrenia and Healthy Aging: Testing the Accelerated Aging Hypothesis of Schizophrenia.
Islam, F, Mulsant, BH, Voineskos, AN, Rajji, TK
Current psychiatry reports. 2017;(7):36
Abstract
PURPOSE OF REVIEW Schizophrenia has been hypothesized to be a syndrome of accelerated aging. Brain plasticity is vulnerable to the normal aging process and affected in schizophrenia: brain-derived neurotrophic factor (BDNF) is an important neuroplasticity molecule. The present review explores the accelerated aging hypothesis of schizophrenia by comparing changes in BDNF expression in schizophrenia with aging-associated changes. RECENT FINDINGS Individuals with schizophrenia show patterns of increased overall mortality, metabolic abnormalities, and cognitive decline normally observed later in life in the healthy population. An overall decrease is observed in BDNF expression in schizophrenia compared to healthy controls and in older individuals compared to a younger cohort. There is a marked decrease in BDNF levels in the frontal regions and in the periphery among older individuals and those with schizophrenia; however, data for BDNF expression in the occipital, parietal, and temporal cortices and the hippocampus is inconclusive. Accelerated aging hypothesis is supported based on frontal regions and peripheral studies; however, further studies are needed in other brain regions.
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Obesity and Metabolic Syndrome Affect the Cholinergic Transmission a nd Cognitive Functions.
Martinelli, I, Tomassoni, D, Moruzzi, M, Traini, E, Amenta, F, Tayebati, SK
CNS & neurological disorders drug targets. 2017;(6):664-676
Abstract
BACKGROUND Worldwide, at least 2.8 million people die each year as a result of being overweight or obese. Obesity leads to metabolic syndrome, a pathological condition characterized by adverse metabolic effects on blood pressure, cholesterol, triglycerides and insulin resistance. Population- based investigations have suggested that obesity and metabolic syndrome may be associated with poorer cognitive performance. METHOD A structured search of bibliographic source (PubMed) was undertaken. The following terms "inflammation and obesity and brain", "cholinergic system and obesity", "cholinergic system and metabolic syndrome", "Cognitive impairment and obesity" and "metabolic syndrome and brain" were used as search strings. RESULTS Over 200 papers, mainly published in the past 10 years were analysed. The major results regarded keyword "metabolic syndrome and brain" followed by, "Cognitive impairment and obesity", "inflammation and obesity and brain", "cholinergic system and obesity" and "cholinergic system and metabolic syndrome". Most papers were pre-clinical but, in general, they were inhomogeneous. Therefore, the results were cited according their contribution to clarify the molecular involvement of obesity and/or metabolic syndrome in cholinergic impairment. CONCLUSION This review focuses on the correlation between brain cholinergic system alterations and high-fat diet, describing the involvement of cholinergic system in inflammatory processes related to metabolic syndrome and obesity, which may lead to cognitive decline. Metabolic syndrome has been suggested as a risk factor for cerebrovascular diseases and has been associated with cognitive impairment in different functional brain domains. Preclinical and clinical studies have identified the cholinergic system as a specific target of metabolic syndrome and obesity. The modifications of cholinergic neurotransmission and its involvement in neuro-inflammation may be related to cognitive impairment that affects obese patients.
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The impact of diet-based glycaemic response and glucose regulation on cognition: evidence across the lifespan.
Sünram-Lea, SI, Owen, L
The Proceedings of the Nutrition Society. 2017;(4):466-477
Abstract
The brain has a high metabolic rate and its metabolism is almost entirely restricted to oxidative utilisation of glucose. These factors emphasise the extreme dependence of neural tissue on a stable and adequate supply of glucose. Whereas initially it was thought that only glucose deprivation (i.e. under hypoglycaemic conditions) can affect brain function, it has become apparent that low-level fluctuations in central availability can affect neural and consequently, cognitive performance. In the present paper the impact of diet-based glycaemic response and glucose regulation on cognitive processes across the lifespan will be reviewed. The data suggest that although an acute rise in blood glucose levels has some short-term improvements of cognitive function, a more stable blood glucose profile, which avoids greater peaks and troughs in circulating glucose is associated with better cognitive function and a lower risk of cognitive impairments in the longer term. Therefore, a habitual diet that secures optimal glucose delivery to the brain in the fed and fasting states should be most advantageous for the maintenance of cognitive function. Although the evidence to date is promising, it is insufficient to allow firm and evidence-based nutritional recommendations. The rise in obesity, diabetes and metabolic syndrome in recent years highlights the need for targeted dietary and lifestyle strategies to promote healthy lifestyle and brain function across the lifespan and for future generations. Consequently, there is an urgent need for hypothesis-driven, randomised controlled trials that evaluate the role of different glycaemic manipulations on cognition.
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Metabolic, endocrine, and other genetic disorders.
Dahmoush, HM, Melhem, ER, Vossough, A
Handbook of clinical neurology. 2016;:1221-59
Abstract
Metabolic, endocrine, and genetic diseases of the brain include a very large array of disorders caused by a wide range of underlying abnormalities and involving a variety of brain structures. Often these disorders manifest as recognizable, though sometimes overlapping, patterns on neuroimaging studies that may enable a diagnosis based on imaging or may alternatively provide enough clues to direct further diagnostic evaluation. The diagnostic workup can include various biochemical laboratory or genetic studies. In this chapter, after a brief review of normal white-matter development, we will describe a variety of leukodystrophies resulting from metabolic disorders involving the brain, including mitochondrial and respiratory chain diseases. We will then describe various acidurias, urea cycle disorders, disorders related to copper and iron metabolism, and disorders of ganglioside and mucopolysaccharide metabolism. Lastly, various other hypomyelinating and dysmyelinating leukodystrophies, including vanishing white-matter disease, megalencephalic leukoencephalopathy with subcortical cysts, and oculocerebrorenal syndrome will be presented. In the following section on endocrine disorders, we will examine various disorders of the hypothalamic-pituitary axis, including developmental, inflammatory, and neoplastic diseases. Neonatal hypoglycemia will also be briefly reviewed. In the final section, we will review a few of the common genetic phakomatoses. Throughout the text, both imaging and brief clinical features of the various disorders will be discussed.
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Neurodegeneration with Brain Iron Accumulation.
Schneider, SA
Current neurology and neuroscience reports. 2016;(1):9
Abstract
Syndromes with neurodegeneration with brain iron accumulation (NBIA) are a group of neurodegenerative disorders characterized by abnormalities in brain iron metabolism with excess iron accumulation in the globus pallidus and to a lesser degree in the substantia nigra and sometimes adjacent areas. They clinically present as neurodegenerative diseases with progressive hypo- and/or hyperkinetic movement disorders and a variable degree of pyramidal, cerebellar, peripheral nerve, autonomic, cognitive and psychiatric involvement, and visual dysfunction. Several causative genes underlying NBIA have been identified which explain about 65% of cases. Pathophysiologically, many of the NBIA syndromes map into related biochemical pathways and gene networks including mitochondrial pathways, lipid metabolism, and autophagy. Treatment for NBIA disorders remains symptomatic but a placebo-controlled double-blind study is underway. Rapid developments prompted the review of this interesting field.
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Current status and future challenges of brain imaging with (18)F-DOPA PET for movement disorders.
Calabria, FF, Calabria, E, Gangemi, V, Cascini, GL
Hellenic journal of nuclear medicine. 2016;(1):33-41
Abstract
OBJECTIVE Parkinson's disease (PD) is a neurodegenerative disorder (ND) due to progressive loss of dopaminergic neurons in the basal ganglia. The correct differential diagnosis of this disease with parkinsonian syndromes (PS) or with essential tremor (ET) is a diagnostic dilemma, considering that only PD is responsive to treatment with levodopa. Traditional imaging fails to diagnose PD because morphological alterations in the brain are usually detectable only at advanced stages. Single photon emission tomography (SPET) with cocaine analogues has recently been used in the early detection of PD. The fluoro-18-deoxyphenyl-alanine ((18)F-DOPA) is a positron emission tomography (PET) tracer with selective in vivo affinity to the basal ganglia, due to the specific metabolism of substantia nigra. We assessed the effective use of (18)F-DOPA PET in brain imaging in order to describe the function of presynaptic disorders of PD, PS, ET and other movement disorders compared to SPET imaging and also discussed novel radiopharmaceuticals. The role of magnetic resonance imaging (MRI) was also discussed. CONCLUSION (18)F-DOPA PET imaging is still the best diagnostic tool for the diagnosis of PD and other movement disorders. Fluorine-18-FDG PET can play a role in the differential diagnosis between PD and other PS. The hybrid (18)F-DOPA PET/MRI seems to be able to play an important additional role in early diagnosis of the above syndromes.
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Schizophrenia and the gut-brain axis.
Nemani, K, Hosseini Ghomi, R, McCormick, B, Fan, X
Progress in neuro-psychopharmacology & biological psychiatry. 2015;:155-60
Abstract
Several risk factors for the development of schizophrenia can be linked through a common pathway in the intestinal tract. It is now increasingly recognized that bidirectional communication exists between the brain and the gut that uses neural, hormonal, and immunological routes. An increased incidence of gastrointestinal (GI) barrier dysfunction, food antigen sensitivity, inflammation, and the metabolic syndrome is seen in schizophrenia. These findings may be influenced by the composition of the gut microbiota. A significant subgroup of patients may benefit from the initiation of a gluten and casein-free diet. Antimicrobials and probiotics have therapeutic potential for reducing the metabolic dysfunction and immune dysregulation seen in patients with schizophrenia.
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Dietary proteins and IGF I levels in preterm infants: determinants of growth, body composition, and neurodevelopment.
Yumani, DF, Lafeber, HN, van Weissenbruch, MM
Pediatric research. 2015;(1-2):156-63
Abstract
It has been demonstrated that a high-protein diet in preterm born infants during the first weeks of life may enable a growth rate equal to that seen in utero and may also result in a better long-term neurodevelopmental outcome. This diet may limit immediate postnatal growth retardation and may hence lower the risk of increased fat deposition after birth leading to the metabolic syndrome in later life. Insulin-like growth factor I (IGF I) has proven to play an important role in early postnatal growth of preterm infants, but also seems to have a persisting influence on body composition in childhood. Furthermore, increased IGF I concentrations in preterm infants have been associated with improved neurodevelopmental outcome. This review will elaborate on the role of dietary proteins and IGF I on growth, body composition, and neurodevelopment of preterm infants. Possible causal pathways will be explored and areas for future research will be proposed.