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Novel roles of non-coding brain RNAs in health and disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889193097 Year: Pages: 213 DOI: 10.3389/978-2-88919-309-7 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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Non-coding RNAs (ncRNAs), and in particular microRNAs are rapidly becoming the focus of research interest in numerous basic and translational fields, including brain research; and their importance for many aspects in brain functioning merits special discussion. The wide-scope, multi-targeted and highly efficient manner of ncRNA regulatory activities draws attention to this topic by many, but the available research and analysis tools and experimental protocols are still at their infancy, and calls for special discussion given their importance for many aspects in brain functioning. This eBook is correspondingly focused on the search for, identification and exploration of those non-coding RNAs whose activities modulate the multi-leveled functions of the eukaryotic brain. The different articles strive to cover novel approaches for identifying and establishing ncRNA-target relationships, provide state of the art reports of the affected neurotransmission pathways, describe inherited and acquired changes in ncRNA functioning and cover the use of ncRNA mimics and blockade tools for interference with their functions in health and disease of the brain. Non-coding RNAs are here to stay, and this exciting eBook provides a glimpse into their impact on our brain’s functioning at the physiology, cell biology, behavior and immune levels.

Amyloid-beta clearance in Alzheimer's disease

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194438 Year: Pages: 111 DOI: 10.3389/978-2-88919-443-8 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-02-05 17:24:33
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Strong evidence continues to accumulate indicating that amyloid-beta (Aß) is a central part of Alzheimer’s disease (AD) pathogenesis in spite of the negative evidence coming from failed clinical trials. Therefore, mechanisms of clearance of Aß are of great interest in understanding AD pathogenesis and the development of effective treatments. This topic focuses on the issues related to Aß clearance in AD. The topics covered include proteases that degrade Aß and their localization, regulation, and functions. This topic also covers issues related to clearance through uptake by glia and through low-density lipoprotein (LDL) receptor mediated mechanisms. Signal transduction related to AD pathology and clearance is also addressed. Finally, immunotherapy and other novel therapeutic approaches are discussed.

Metals and neurodegeneration: Restoring the balance

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197392 Year: Pages: 132 DOI: 10.3389/978-2-88919-739-2 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Biometals such as copper, zinc and iron have key biological functions, however, aberrant metabolism can lead to detrimental effects on cell function and survival. These biometals have important roles in the brain, driving cellular respiration, antioxidant activity, intracellular signaling and many additional structural and enzymatic functions. There is now considerable evidence that abnormal biometal homeostasis is a key feature of many neurodegenerative diseases and may have an important role in the onset and progression of disorders such as Alzheimer’s, Parkinson’s, prion and motor neuron diseases. Recent studies also support biometal roles in a number of less common neurodegenerative disorders. The role of biometals in a growing list of brain disorders is supported by evidence from a wide range of sources including molecular genetics, biochemical studies and biometal imaging. These studies have spurred a growing interest in understanding the role of biometals in brain function and disease as well as the development of therapeutic approaches that may be able to restore the altered biometal chemistry of the brain. These approaches range from genetic manipulation of biometal transport to chelation of excess metals or delivery of metals where levels are deficient. A number of these approaches are offering promising results in cellular and animal models of neurodegeneration with successful translation to pre-clinical and clinical trials. At a time of aging populations and slow progress in development of neurotherapeutics to treat age-related neurodegenerative diseases, there is now a critical need to further our understanding of biometals in neurodegeneration. This issue covers a broad range of topics related to biometals and their role in neurodegeneration. It is hoped that this will inspire greater discussion and exchange of ideas in this crucial area of research and lead to positive outcomes for sufferers of these neurodegenerative diseases.

The Metaphorical Brain

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197729 Year: Pages: 178 DOI: 10.3389/978-2-88919-772-9 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2016-04-07 11:22:02
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Metaphor has been an issue of intense research and debate for decades (see, for example [1]). Researchers in various disciplines, including linguistics, psychology, computer science, education, and philosophy have developed a variety of theories, and much progress has been made [2]. For one, metaphor is no longer considered a rhetorical flourish that is found mainly in literary texts. Rather, linguists have shown that metaphor is a pervasive phenomenon in everyday language, a major force in the development of new word meanings, and the source of at least some grammatical function words [3]. Indeed, one of the most influential theories of metaphor involves the suggestion that the frequency of metaphoric language results because cross-domain mappings are a major determinant in the organization of semantic memory, as cognitive and neural resources for dealing with concrete domains are recruited for the conceptualization of more abstract ones [4]. Researchers in cognitive neuroscience have explored whether particular kinds of brain damage are associated with metaphor production and comprehension deficits, and whether similar brain regions are recruited when healthy adults understand the literal and metaphorical meanings of the same words (see [5] for a review). Whereas early research on this topic focused on the issue of the role of hemispheric asymmetry in the comprehension and production of metaphors [6], in recent years cognitive neuroscientists have argued that metaphor is not a monolithic category, and that metaphor processing varies as a function of numerous factors, including the novelty or conventionality of a particular metaphoric expression, its part of speech, and the extent of contextual support for the metaphoric meaning (see, e.g., [7], [8], [9]). Moreover, recent developments in cognitive neuroscience point to a sensorimotor basis for many concrete concepts, and raise the issue of whether these mechanisms are ever recruited to process more abstract concepts [10]. This Frontiers Research Topic brings together contributions from researchers in cognitive neuroscience whose work involves the study of metaphor in language and thought in order to promote the development of the neuroscientific investigation of metaphor. Adopting an interdisciplinary perspective, it synthesizes current findings on the cognitive neuroscience of metaphor, provides a forum for voicing novel perspectives, and promotes avenues for new research on the metaphorical brain.

Omega-3 Fatty Acids in Health and Disease

ISBN: 9783038422723 9783038422730 Year: Pages: XII, 312 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Medicine (General)
Added to DOAB on : 2016-11-11 19:02:10
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The role of major dietary omega-3 fatty acids (Ω-3; α-linolenic acid, eicosapentaenoic acid and docosahexaenoic acid) in human health has generated enormous scientific interest and many controversies in recent years. Due to a growing number of studies with conflicting or even negative clinical results, the former “hype” of Ω-3 thought to be beneficial in many aspects of human health regardless of the physiological and clinical preconditions is now being critically re-evaluated, especially with respect to the potential role of Ω-3 fatty acid supplementation in preventing a variety of diseases and clinical conditions. This critical view reflects the complex interaction of Ω-3 with cell membranes and their integrated proteins mediating signal transduction, transport systems, and other processes. Moreover, Ω-3 are precursors of bioactive metabolites, such as eicosanoids, lipoxins, resolvins, protectins, maresins, and nitrolipids that influence several physiological and pathophysiological processes and their full spectrum of effects are only beginning to be defined. Finally, physiological and pathophysiological conditions as well as concomitant pharmacological treatments may influence the specific and non-specific actions of Ω-3 supplementation.This Special Issue of the Journal of Clinical Medicine will emphasize the role and biological interactions of Ω-3 with regard to cancer, psychiatric disorders, metabolic disorders and nutrition and will also reflect on some basic molecular and cellular mechanisms.

ICT for assessment and rehabilitation in Alzheimer's disease and related disorders

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889197781 Year: Pages: 170 DOI: 10.3389/978-2-88919-778-1 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2017-02-03 17:04:57
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Information and Communication Technologies (ICT) are no longer objects gathering dust on a shelf; instead, they have become intrinsic in our everyday lives. They are now even taking on an indispensable role in many clinical and rehabilitation settings. In the past decade there has been a surge of interest in using ICT with elderly people, both with and without dementia, in various clinical and research settings. On the one hand, ICT can supplement the assessment of functional ability by more precisely evaluating the nature and extent of functional impairment; on the other hand, ICT can be used to support elderly people in their everyday activities, as well as to ameliorate symptoms and improve quality of life through stimulation and rehabilitation. This is the intention driving the development of Serious Games (SG), which are digital applications (often based on Virtual Reality) specifically adapted for purposes other than entertaining, including rehabilitation, training and education. Finally, ICT can also play a key role in the development of interactive educational programs to support caregivers of people living with dementia. A handful of interesting studies have started to investigate the effectiveness of employing ICT in people with different types of dementia, such as Alzheimer’s disease (AD). It is therefore timely to attempt to scope this newly emerging field, as well as to foster a dialogue among the different professionals, including academics, clinicians and computer engineers, working in the area. With this in mind, the Research Topic “ICT for assessment and rehabilitation in Alzheimer’s disease and related disorders” aims to provide new and interesting insights into the current use of ICT in healthy and pathological aging. The intent is also to identify challenges and new perspectives in the field, gather recommendations for the application of ICT in AD and related disorders in clinical practice, and to showcase cutting edge clinical research. The articles included in this Frontier Research Topics have more than achieved this aim and are a perfect illustration of how ICT can be used to enhance the lives of people living dementia and their caregivers.

Intellectual Disabilities in Down Syndrome from Birth and throughout Life: Assessment and Treatment

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450459 Year: Pages: 179 DOI: 10.3389/978-2-88945-045-9 Language: English
Publisher: Frontiers Media SA
Subject: Neurology --- Science (General)
Added to DOAB on : 2017-07-06 13:27:36
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Research on the multiple aspects of cognitive impairment in Down syndrome (DS), from genes to behavior to treatment, has made tremendous progress in the last decade. The study of congenital intellectual disabilities such as DS is challenging since they originate from the earliest stages of development and both the acquisition of cognitive skills and neurodegenerative pathologies are cumulative. Comorbidities such as cardiac malformations, sleep apnea, diabetes and dementia are frequent in the DS population, as well, and their increased risk provides a means of assessing early stages of these pathologies that is relevant to the general population. Notably, persons with DS will develop the histopathology of Alzheimer’s disease (formation of neuritic plaques and tangles) and are at high risk for dementia, something that cannot be predicted in the population at large. Identification of the gene encoding the amyloid precursor protein, its localization to chromosome 21 in the 90’s and realization that all persons with DS develop pathology identified this as an important piece of the amyloid cascade hypothesis in Alzheimer’s disease. Awareness of the potential role of people with DS in understanding progression and treatment as well as identification of genetic risk factors and also protective factors for AD is reawakening. For the first time since DS was recognized, major pharmaceutical companies have entered the search for ameliorative treatments, and phase II clinical trials to improve learning and memory are in progress. Enriched environment, brain stimulation and alternative therapies are being tested while clinical assessment is improving, thus increasing the chances of success for therapeutic interventions. Researchers and clinicians are actively pursuing the possibility of prenatal treatments for many conditions, an area with a huge potential impact for developmental disorders such as DS. Our goal here is to present an overview of recent advances with an emphasis on behavioral and cognitive deficits and how these issues change through life in DS. The relevance of comorbidities to the end phenotypes described and relevance of pharmacological targets and possible treatments will be considerations throughout.Research on the multiple aspects of cognitive impairment in Down syndrome (DS), from genes to behavior to treatment, has made tremendous progress in the last decade. The study of congenital intellectual disabilities such as DS is challenging since they originate from the earliest stages of development and both the acquisition of cognitive skills and neurodegenerative pathologies are cumulative. Comorbidities such as cardiac malformations, sleep apnea, diabetes and dementia are frequent in the DS population, as well, and their increased risk provides a means of assessing early stages of these pathologies that is relevant to the general population. Notably, persons with DS will develop the histopathology of Alzheimer’s disease (formation of neuritic plaques and tangles) and are at high risk for dementia, something that cannot be predicted in the population at large. Identification of the gene encoding the amyloid precursor protein, its localization to chromosome 21 in the 90’s and realization that all persons with DS develop pathology identified this as an important piece of the amyloid cascade hypothesis in Alzheimer’s disease. Awareness of the potential role of people with DS in understanding progression and treatment as well as identification of genetic risk factors and also protective factors for AD is reawakening. For the first time since DS was recognized, major pharmaceutical companies have entered the search for ameliorative treatments, and phase II clinical trials to improve learning and memory are in progress. Enriched environment, brain stimulation and alternative therapies are being tested while clinical assessment is improving, thus increasing the chances of success for therapeutic interventions. Researchers and clinicians are actively pursuing the possibility of prenatal treatments for many conditions, an area with a huge potential impact for developmental disorders such as DS. Our goal here is to present an overview of recent advances with an emphasis on behavioral and cognitive deficits and how these issues change through life in DS. The relevance of comorbidities to the end phenotypes described and relevance of pharmacological targets and possible treatments will be considerations throughout.

Biology of Cognitive Aging: Model Systems, Technologies and Beyond

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889451449 Year: Pages: 145 DOI: 10.3389/978-2-88945-144-9 Language: English
Publisher: Frontiers Media SA
Subject: Genetics --- Science (General)
Added to DOAB on : 2017-07-06 13:27:36
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Welcome! We, humans, tend to experience forgetfulness when we get old. The forgetfulness may become more serious memory impairment, dementia. Presumably, we have known it for a long time, but we still do not know the mechanism behind. A normal part of forgetfulness is called age-related memory impairment (AMI), which is considered the first step towards mild cognitive impairment (MCI; transition state) and dementia (disease state). The majority of dementia is attributable to Alzheimer’s disease (AD). Progression to dementia occurs at a high rate in patients with AMI. This eBook covers exciting but yet challenging field of cognitive aging. AMI is specific to neural tissues of the brain and is considered to be segmental aging. It happens not only to humans but also to a variety of species. Learning and memory are vulnerable to aging in a wide variety of model species, including worms, fruit flies, insects, snails, fishes, and rodents. Aging specifically reduces the ability to learn new information but leaves “old” memories and procedural memory intact. A comparative approach including the use of model systems seems to facilitate understanding of the molecular mechanisms that lead to AMI and AD. We advocate research on model systems. This eBook also provides the first manuscript co-authored with an AD patient to create a feedback loop from patients incorporated into research. We also included a manuscript on the semi-automated system that was inspired by such a feedback. Those may place a nice flavor to this exciting series of comparative research on cognitive aging. We hope you enjoy this eBook. Warm regards, Shin Murakami, Ph.D.Welcome! We, humans, tend to experience forgetfulness when we get old. The forgetfulness may become more serious memory impairment, dementia. Presumably, we have known it for a long time, but we still do not know the mechanism behind. A normal part of forgetfulness is called age-related memory impairment (AMI), which is considered the first step towards mild cognitive impairment (MCI; transition state) and dementia (disease state). The majority of dementia is attributable to Alzheimer’s disease (AD). Progression to dementia occurs at a high rate in patients with AMI. This eBook covers exciting but yet challenging field of cognitive aging. AMI is specific to neural tissues of the brain and is considered to be segmental aging. It happens not only to humans but also to a variety of species. Learning and memory are vulnerable to aging in a wide variety of model species, including worms, fruit flies, insects, snails, fishes, and rodents. Aging specifically reduces the ability to learn new information but leaves “old” memories and procedural memory intact. A comparative approach including the use of model systems seems to facilitate understanding of the molecular mechanisms that lead to AMI and AD. We advocate research on model systems. This eBook also provides the first manuscript co-authored with an AD patient to create a feedback loop from patients incorporated into research. We also included a manuscript on the semi-automated system that was inspired by such a feedback. Those may place a nice flavor to this exciting series of comparative research on cognitive aging. We hope you enjoy this eBook. Warm regards, Shin Murakami, Ph.D.

Neurodegeneration: From Genetics to Molecules

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889450206 Year: Pages: 264 DOI: 10.3389/978-2-88945-020-6 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2018-02-27 16:16:44
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Chronic degenerative diseases are one of the major public health problems, particularly those affecting the nervous system. They are characterized by the degeneration of specific cell populations that include several pathologies which contribute significantly to morbidity and mortality in the elderly population. Therefore, in recent years, the study of neuroscience has gained significant importance. Most of these neurodegenerative disorders are the result of a complex interaction between genetic and environmental factors that generate progression and can even determine its severity. The presence of mutations in genes as LRRK2, SNCA, PARK7, PARK2 or PINK1 is associated with Parkinson's disease. Mutations in genes such as APP, PS1 and PS2 are associated with familial Alzheimer's disease; while HTT gene mutations are the cause of Huntington's disease. In most cases, this condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. It is known that these mutations can also alter the proteins function; however, it has not yet been possible to fully understand how some genetic changes cause the disease or influence the risk of developing these disorders. Most symptoms seen in these conditions occurs when specific nerve cells are damaged or die generating a loss in brain communication. Also many of these mutations generate aggregation of intracellular or extracellular proteins affecting cell function and eventually causing neuronal death. It is unclear whether the presence of these aggregates play an important role in nerve cell death during the development of neurodegenerative diseases, or if they are simply part of the response of cells to the disease. Other mutations affect the mitochondrial function generating alterations in energy production and promoting the formation of unstable molecules such as free radicals. Under normal conditions, the harmful effects caused by free radicals, are offset within the cell. However, in pathological conditions, the presence of mutations can alter this process by allowing the accumulation of radicals and damaging or killing cells. On the other hand, we also know that these diseases may not have a direct genetic component, thus, the study of sporadic type neurodegenerative diseases is much more complex. Histopathological lesions as well as the cellular and molecular alterations are generally indistinguishable from familial cases. For this reason, it is important to understand the genetic and molecular mechanisms associated with this type of pathologies. In this sense, this issue aims to understand the molecular processes that occur in the brain, and how these are influenced by the environment, genetics and behavior.

The Metabolic-Inflammatory Axis in Brain Aging and Neurodegeneration

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889452538 Year: Pages: 161 DOI: 10.3389/978-2-88945-253-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2018-02-27 16:16:44
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Impairment of energy metabolism is a hallmark of brain aging and several neurodegenerative diseases, such as the Alzheimer’s disease (AD). Age- and disease-related hypometabolism is commonly associated with oxidative stress and they are both regarded as major contributors to the decline in synaptic plasticity and cognition. Neuroinflammatory changes, entailing microglial activation and elevated expression of inflammatory cytokines, also correlate with age-related cognitive decline. It is still under debate whether the mitochondrial dysfunction-induced metabolic deficits or the microglia activation-mediated neuroinflammation is the initiator of the cognitive changes in aging and AD. Nevertheless, multiple lines of evidence support the notion that mitochondrial dysfunction and chronic inflammation exacerbate each other, and these mechanistic diversities have cellular redox dysregulation as a common denominator. This research topic focuses on the role of a metabolic-inflammatory axis encompassing the bioenergetic activity, brain inflammatory responses and their redox regulation in healthy brain aging and neurodegenerative diseases. Dynamic interactions among these systems are reviewed in terms of their causative or in-tandem occurrence and how the systemic environment, –e.g., insulin resistance, diabetes, and systemic inflammation–, impacts on brain function.

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