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Unraveling Neuroprotective and Neurodegenerative Signals in Neurodegeneration

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199563 Year: Pages: 131 DOI: 10.3389/978-2-88919-956-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-01-19 14:05:46
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Proteinopathy is a collective term used to classified neurodegenerative diseases associated with the progressive accumulation of toxic protein molecules in specific brain regions. Alzheimer’s disease (AD) is a well-known proteinopathy characterize by the accumulation of A peptides and tau proteins. The accumulation of these toxic molecules in the brain starts many years before any clinical presentation, being the onset in the range of 65 to 72 years of age. Therefore, age is considered a risk factor due, in part, to the loss of molecular competence to clear the brain from these toxic protein molecules. This fact, supported by years of research, demonstrates that brain cells activate a neuroprotective mechanism upon detection of a pathobiological signal that (if the detrimental conditions persist) precedes the activation of the neurodegeneration pathway. The progressive brain region specific neuronal death in neurodegenerative diseases also indicates that the transition from neuroprotection to neurodegeneration is individually triggered in cells of the affected brain region. Thus, molecular understanding of the pathophysiology associated with proteinopathies needs to take in consideration this intricate transition process, especially when genomics and proteomics approaches are used. Research directed to understand the pathogenesis and pathophysiology of neurodegenerative diseases uncovered the putative role of different molecular mechanisms associated with neurodegeneration. Among the molecular mechanisms identified are proteolysis, epigenetics, microRNA, transcriptional regulation, innate and adaptive immune system, phagocytosis and autophagocytosis, exo/endocytosis, unfolded protein response, cytoskeleton defects, unregulated signaling molecules (i.e. kinases and phosphatases), trafficking molecules, cell cycle, neurogenesis/neurodevelopment, among others. Interestingly, all these molecular mechanisms have been identified through the analysis of tissue from animal models or human post-mortem pathologically confirmed cases, but their specific role in neurodegeneration is still unclear. Thus, it is plausible to consider that all these pathways play a role at a particular phase of the neurodegeneration process or, simply, are drive by the agonal state of the tissue examined. Hence, an important conundrum that researchers face today is the use of heterogeneous brain tissue samples in the quest to identify biomarkers associated with the pathogenesis or pathophysiology of neurodegenerative diseases. At this junction of the neurodegeneration field, this research topic aim to critically assess the current literature on molecular mechanisms associated with neurodegeneration and the approaches used to dissect their putative pathophysiological role. The studies could include the interplay between neuroprotective and neurodegenerative signals in neurodegeneration, dissecting the molecular role of identified biomarkers, bioinformatics tools that facilitate data mining, dissecting pathways or molecular mechanisms, stages of protein aggregation (oligomers vs tangles; who did it?), aging brain and brain fitness (A natural selection process), adaptive protein response to environmental insults and cellular signals, expression profile associated with neurological disorders and health. Therefore, this Research Topic is expected to cover a wide range of subjects related to unravel the interplay between neuroprotective and neurodegenerative signals in neurodegeneration.

Nicotinic Acetylcholine Receptor Signaling in Neuroprotection

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ISBN: 9789811084874 9789811084881 Year: Pages: 191 DOI: https://doi.org/10.1007/978-981-10-8488-1 Language: English
Publisher: Springer Grant: Smoking Research Foundation
Subject: Neurology
Added to DOAB on : 2018-06-29 14:19:40
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This open access book presents the roles and mechanisms of signal transduction triggered by nicotinic acetylcholine receptors (nAChRs) stimulation in neuroprotection against toxic effects of risk factors of neurodegenerative diseases. Accumulating evidence suggests that nAChRs in the CNS play important roles not only in excitatory neurotransmission but also in neuronal survival and related functions. Neuroprotection mediated by nAChRs in neurodegenerative diseases such as Alzheimer's disease is the major topic of this book. In response to rapidly evolving areas in clinical and laboratory neuropharmacology and neurochemistry, this volume provides in-depth coverage of neuroprotection in basic research and future developments in the clinical application of effective neuroprotective strategies in neurodegenerative diseases. This work appeals to both basic and clinical researchers in several fields, such as neuroscience, neurology, and pharmacology.

Preclinical and clinical issues in Alzheimer's disease drug research and development

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889194339 Year: Pages: 100 DOI: 10.3389/978-2-88919-433-9 Language: English
Publisher: Frontiers Media SA
Subject: Therapeutics --- Science (General)
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Alzheimer’s disease (AD) is a chronic neurodegenerative disorder characterized by progressive cognitive dysfunction and memory loss, inability to perform the activities of daily living and mood disorders. According to the so-called “amyloid cascade hypothesis”, amyloid-ß- peptide (Aß), produced by beta- and gamma- secretase-mediated cleavages of the amyloid precursor protein (APP), plays a pivotal role in the pathogenesis of AD. Aß was also shown to contribute to AD pathology by stimulating the hyperphosphorylation of tau which is responsible for the formation of neurofibrillary tangles. However, the “amyloid cascade hypothesis” was challenged by other theories which lend support to the idea that Aß is not causative but can be considered as an “innocent bystander” in AD. Although preclinical research generated impressive lines of evidence about the several intracellular mechanism(s) whose impairment leads to the onset and progression of AD, clinical research aimed at the development of new drugs capable of preventing or delaying the onset of neuronal damage in AD patients has produced limited results. The drugs currently available for the treatment of AD are acetylcholinesterase inhibitors (AChEI) and the NMDA glutamate receptor antagonist memantine. The AChEI increase acetylcholine levels in the synaptic cleft, which are reduced because of the progressive damage of cholinergic neurons in cognitive brain areas (e.g. amygdala, hippocampus, and frontal cortex), whereas memantine is used to prevent/reduce calcium-dependent excitotoxic neuronal cell death. Both classes of drugs have been shown to improve symptoms related to cognitive decline, but their effects are confined largely to patients with mild to moderate AD, in particular during the first year or so of treatment. An alternative to this symptomatic treatments involves the use of drugs that intervene in the pathogenesis of the disease. Recently, monoclonal antibodies against Aß were proposed as novel agents capable to remove Aß from the brain thus preventing neuronal damage. The research topic focuses on the preclinical and clinical evidence about the several factors that contribute to the pathogenesis of AD as well as the potential therapeutic role of new classes of drugs still under preclinical or clinical development.

Neurophysiology in Alzheimer's Disease and Dementia

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199303 Year: Pages: 106 DOI: 10.3389/978-2-88919-930-3 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-01-19 14:05:46
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Alzheimer's disease (AD) and dementia are the most common neurodegenerative disorder. Since the number of individuals with AD and dementia is expected to increase considerably in the near future, reliable treatment and diagnosis are critical. EEG and neurophysiological technique could be used as a cost-effective screening tool for early detection and diagnosis in the Mild Cognitive Impairment (MCI) stage. The aim in neurophysiology research is to develop signal processing methods that improve the specificity for diagnosing dementia; we wish to discover signal features that not only significantly differ in AD patients, but also allow us to reliably separate AD patients and control subjects. This approach is valuable for clinical purposes (as diagnostic tool for dementia), and it also more fundamentally contributes to a better understanding of brain dynamics of MCI patients. Finally, the development of neurophysiological biomarker could be useful in monitoring pharmacological treatments. The main focus of this special issue will be on the most recent developments and ideas in the field of EEG and neurophysiology which will enable us to extract features that improve the specificity for diagnosing AD and dementia.

Alzheimer's Disease and the Fornix

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889199594 Year: Pages: 110 DOI: 10.3389/978-2-88919-959-4 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-01-19 14:05:46
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This e-book focuses primarily on the role of the fornix as a functional, prognostic, and diagnostic marker of Alzheimer’s disease (AD), and the application of such a marker in clinical practice. Researchers have long been focused on the cortical pathology of AD, since the most important pathologic features are the senile plaques found in the cortex, and the neurofibrillary tangles and neuronal loss that start from the entorhinal cortex and the hippocampus. In addition to gray matter structures, histopathological studies indicate that the white matter is also altered in AD. The fornix is a white matter bundle that constitutes a core element of the limbic circuits, and is one of the most important anatomical structures related to memory. The fornices originate from the bilateral hippocampi, merge at the midline of the brain, again divide into the left and right side, and then into the precommissural and the postcommissural fibers, and terminate at the septal nuclei, nucleus accumbens (precommissural fornix), and hypothalamus (postcommissural fornix). These functional and anatomical features of the fornix have naturally captured researchers’ attention as possible diagnostic and prognostic markers of AD. Growing evidence indicates that the alterations seen in the fornix are potentially a good marker with which to predict future conversion from mild cognitive impairment to AD, and even from a cognitively normal state to AD. The degree of alteration is correlated with the degree of memory impairment, indicating the potential for the use of the fornix as a functional marker. Moreover, there have been attempts to stimulate the fornix to recover the cognitive function lost with AD. Our goal is to provide information about the status of current research and to facilitate further scientific and clinical advancement in this topic.

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.

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.

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