Among neurodegenerative diseases, those that lead to a state of dementia are the aim of several investigations. Dementia is a chronic disease the prevalence of which is increasing worldwide. The number of dementia patients in the world is approximately 50 million, and it is estimated that the number of patients will reach 131.5 million by 2050. This increase will be accompanied by a significant increase in medical expenditures and other expenses, especially for elderly patients. Therefore, the maintenance cost of dementia in the future is expected to be quite high. For this reason, several investigations aim, firstly, to describe the key mechanisms involved in the origin of dementia and, secondly, to establish preventive and therapeutic strategies in order to understand and mitigate this debilitating pathology. <p> This volume of Frontiers in Clinical Drug Research - Dementia explores the current comorbidities that cause cognitive impairment and the current management alternatives for clinical cases of dementia. The reviews contributed in these volume will provide readers with a current perspective on the subject. The topics covered in this volume include: <p> - Comorbidities inducing mild cognitive impairment - an evaluation of the risk caused by some pathological conditions <p> - Tau-targeted therapy in Alzheimer's disease - history and current state <p> - Emerging nanotherapeutic strategies in Alzheimer's disease <p> - Implication of dehydroepiandrosterone on dementia related to oxidative stress <p> - Polyphenol compounds as potential therapeutic agents in Alzheimer’s disease <p> The volume is a timely update on dementia treatment for clinical physicians, neurologists, gerontologists, pharmaceutical and medicinal chemistry researchers, and physiologists.

This e-book is a reference on Selegiline/(-)-Deprenyl effects on the brain. Selegiline, described in thousands of research papers, is registered in over 60 countries. At present, more than one hundred preparations containing selegiline circulate in the global market under different brand names. They are widely used in the treatment of Parkinson’s disease, Alzheimer’s disease, major depression and as a geroptotective / anti-aging drug. (-)-Deprenyl/selegiline, the first selective inhibitor of B-type MAO which, in contrast to the known MAO inhibitors, did not potentiate the effect of tyramine but inhibited it. The compound could be combined with levodopa in Parkinson’s disease without signs of hypertensive reactions. The DATATOP study in the USA revealed that (-)-deprenyl delayed the onset of disability associated with early, otherwise untreated Parkinson’s disease. The age-related decay of the supply of the brain with phenylethylamine ( PEA), due to the progressive increase of MAO-B activity in the aging brain, and dopamine, due to the better than average decline of the dopaminergic neuronal activity during the postdevelopmental phase of life, are irresistible biochemical lesions of aging. The speed of deterioration of behavioral performances with the passing of time and longevity depends significantly on the pace of the worsening of these leasions. (-)-Deprenyl, Increasing the supply of the brain with PEA and dopamine, counteracts this aging process. Maintenance of male rats from sexual maturity until death on (-)-deprenyl delays the age-related loss of the capacity to ejaculate, slows the age-related decline of learning ability and prolongs life. In humans, maintenance from sexual maturity on (-)-deprenyl (1 mg daily) is, for the time being, the most promising prophylactic treatment to fight against the age-related decay of behavioral performances, prolonging life, and preventing or delaying the onset of age-related neurodegenerative diseases such as Parkinson’s and Alzheimer’s. This e-book is a useful reference for graduate medical students, academic researchers in the field of neuropsychopharmacology, neurophysiology and gerontology and professional research groups in commercial organizations manufacturing selegiline preparations.

Language is the most versatile and fascinating of all human cognitive functions, constituting a field of interest in very different areas, from Linguistics to Speech Therapy, from Philosophy to Computational Sciences, including Psychology, Neurology, Biology, and Social Sciences. The scope of this E-book is to provide the reader with an update on topics relevant to neurolinguistics such as new cognitive models of comprehension and production of normal language, new perspectives on the understanding of aphasic symptoms and the interface between language and other cognitive functions – functional neuroimaging and language. This E-book will be of interest both for teachers and researchers in Neurosciences and Linguistics as well as for professionals who treat patients with disorders of language and communication, such as Neurologists, Psychiatrists, Psychologists, Neuropsychologists, Speech Therapists, and Occupational Therapists, among many others.

Since the last century, remarkable advances at both the basic and clinical levels have considerably improved our ability to evaluate and treat children with neurological disorders. Many cases seen by general pediatricians are primarily neurological accounting for up to 30% of all consultations to pediatrics with a high ratio of follow-up visits to new patients of about 3:1. This manual is a neurology reference for medical students and pediatric residents and is intended to supplement larger textbooks on pediatric neurology already available. Many of undergraduate medical students refer to deficient and oversimplified references that do not enable them to deal with pediatric neurology patients adequately. The manual presents a simplified, organized, and comprehensive problem based approach to common pediatric neurological disorders directed to the level of medical students, pediatric residents, general practitioners and general pediatricians. This e-book is thus a concise outline with practical tips to facilitate proper diagnosis and management of various neurological disorders.

Neurodegenerative diseases are a complex heterogeneous group of diseases associated with site-specific premature and slow death of certain neuronal populations in brain and spinal cord tissues. For example, in Alzheimer disease, neuronal degeneration occurs in the nucleus basalis, whereas in Parkinson disease, neurons in the substantia nigra die. The most severely affected neurons in Huntington disease are striatal medium spiny neurons. The neuronal populations that are lost in neurodegenerative diseases modulate functions such as controlling movements, processing sensory information, memory, and making decisions. Although, the molecular mechanism of neurodegeneration remains unknown, but excitotoxicity, inflammation, and oxidative stress may contribute to neural cell demise independently or synergistically. The purpose of this E-book is to present readers with cutting edge and comprehensive information on molecular aspects of neurodegenerative diseases and neuroprotection in a manner that is useful not only to students and teachers, but also to researchers and physicians.

Stroke is one of the most debilitating diseases which poses a significant economic burden on society. Increasing exposure to behavioural risk factors for stroke (tobacco use, unhealthy diet, physical inactivity and excessive alcohol consumption) and air pollution are driving up the worldwide stroke burden. Although medical interventions to prevent and manage stroke have advanced considerably over the last two decades, they are not consistently implemented worldwide. Therefore, health outcomes of stroke treatment vary throughout the world.

This volume presents a summary of recent research and debates on old and new aspects in stroke medicine. The volume covers topics such as causative factors of stroke such as hypertension, the immune system, genetic factors and the neurovegetative system, to the role of new imaging techniques in improving diagnosis and treatment, from preventive therapy and recanalization to the important and intriguing effects of neuroprotection, neuroregeneration and post stroke rehabilitation. Readers will be able to understand perspectives from stroke medicine researchers about the relationship between the nervous system and other physiological systems in the body and their role in the onset and treatment of stroke. The volume is intended as a resource for neurologists and medical professionals involved in other specialties such as cardiology, internal medicine, rehabilitation and physiology.

The monograph is a summary of methods used to study pain receptors and the results obtained in some experiments designed to study the effect of non-opioid analgesics. The molecular mechanisms of nociceptive information control in primary sensory nociceptive neurons are described based on investigations of the membrane signaling cascade (opioid-like receptor → Na+,K+-ATPase → NaV1.8 channel) observed by the authors. Based on this data, the authors conclude that the modulation of NaV1.8 channels responsible for the coding of noxious signals can be carried out due to two novel targeting mechanisms. The first of these is the activation of opioid-like receptors; the second is the activation of Na+/K+-ATPase as a signal transducer. The development of a novel class of analgesics that trigger these mechanisms should lead to a successful solution to the problem of chronic pain relief. Chapters of the monograph cover the general methods used in studying nociceptive pain (including the patch-clamp method), and the mechanism behind the binding of different ligands to these receptors such gamma-pyrones, gamma-pyridines and cardiotonic steroids. This monograph is a valuable reference for neuroscientists, pharmacologists and allied researchers studying pain receptors for the development of safe and effective analgesics.

Pain is a significant medical problem, as it is a factor in many diseases and debilitating conditions. The processing of pain in the body is a complex process which involves nerve signaling in the milieu of biochemical, molecular and genetic interactions occurring in the brain and other parts of the body. Pain, as a spokesperson of real and impending injury, outlives its usefulness as a warning signal and instead becomes chronic and excruciating. The transition of the realization of pain up to the cortical processing as a persistent condition represents an intricate process governed by the interaction of various factors. Research on humans and animals has led to the advent of personalized medicine where every patient can be treated according to the set of genes they possess. However, the genetic basis for pain has largely been undefined so far. Research on epigenetic alterations and micro-RNA (miRNA) in relation to the assessment and prevention of pain is still in infancy. Pain: Causes, Concerns and Consequences focuses on pain in human diseases such as cardiac and non-cardiac disorders. This compendium on pain research offers basic information and useful updates on the pathology, genetics, and biomolecular pathways that cause pain. Additionally, readers will also learn about non-pharmacological therapies for pain. The monograph is a handy guide for medical students and doctors in different divisions such as oncology, surgery, neurology, psychiatry, psychology, physiotherapy and chiropractic care. The book also serves as a guide for life science researchers who are planning to develop methods to study pain in either a clinical or laboratory setting.

Neurodegenerative disorders such as Amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), Parkinson’s disease (PD), Prion-related disorders (PrD) and Huntington’s disease (HD) share a common neuropathology, primarily featuring the presence of abnormal protein inclusions containing specific misfolded proteins. These groups of diseases are now classified as Protein Misfolding Disorders. This Ebook gives a comprehensive overview of the possible mechanisms involved in Protein Misfolding Disorders and possible therapeutic strategies to treat these diseases. The Ebook provides the most recent evidence addressing the role of cellular stress responses to neurological diseases, along with therapeutic strategies to alleviate ER stress in a disease context.