Glycerophospholipid and sphingolipid-derived lipid mediators facilitate the transfer of messages not only from one cell to another but also from one subcellular organelle to another. These molecules are not only components of neural membranes but also storage depots for lipid mediators. Information on the generation and involvement of lipid mediators in neurological disorders is scattered throughout the literature in the form of original papers and reviews. This book will provide readers with a comprehensive description of glycerophospholipid, sphingolipid and cholesterol-derived lipid mediators and their involvement in neurological disorders.
Glycerophospholipid and sphingolipid-derived lipid mediators facilitate the transfer of messages not only from one cell to another but also from one subcellular organelle to another. These molecules are not only components of neural membranes but also storage depots for lipid mediators. Information on the generation and involvement of lipid mediators in neurological disorders is scattered throughout the literature in the form of original papers and reviews. This book will provide readers with a comprehensive description of glycerophospholipid, sphingolipid and cholesterol-derived lipid mediators and their involvement in neurological disorders.
Lipid Mediators and Their Metabolism in the Brain presents readers with cutting edge and comprehensive information not only on the synthesis and degradation of glycerophospholipid-, sphingolipid-, and cholesterol-derived lipid mediators, but also their involvement in neurological disorders. It is hoped that this monograph will be useful not only to postgraduate student and their teachers, but also to research scientists and physicians, who are curious about the generation and roles of lipid mediators in the brain.
It is becoming increasingly evident that the deficiency of n-3 fatty acids in diet is not only associated with cardiovascular diseases, but also involved in stroke, epilepsy and other neurological and neurodegenerative diseases, such as Alzheimer disease, Parkinson disease, and peroxisomal diseases. In his newest book, Beneficial Effects of Fish Oil on Human Brain, Dr. Akhlaq A. Farooqui expands on the status and therapeutic importance of n-3 fatty acids (major components of fish oil) and their mediators in normal brain and those with neurodegenerative and neuropsychiatric diseases. Farooqui presents the benefits of n-3 fatty acids on Western diet, which is enriched in n-6 fatty acids (major components of vegetable oil) and may promote the above neurological disorders. The book will present readers with cutting edge and comprehensive information on metabolism and roles of neural membrane n-3 fatty acids.
Collectively, neurodegenerative diseases are characterized by chronic and progressive loss of neurons in discrete areas of the brain, producing debilitating symptoms such as dementia, loss of memory, loss of sensory or motor capability, decreased overall quality of life eventually leading to premature death. Two types of cell death are known to occur during neurodegeneration: (a) apoptosis and (b) necrosis. The necrosis is characterized by the passive cell swelling, intense mitochondrial damage with rapid loss of ATP, alterations in neural membrane permeability, high calcium influx, and disruption of ion homeostasis. This type of cell death leads to membrane lysis and release of intracellular components that induce inflammatory reactions. Necrotic cell death normally occurs at the core of injury site. In contrast, apoptosis is an active process in which caspases (a group of endoproteases with specificity for aspartate residues in protein) are stimulated. Apoptotic cell death is accompanied by cell shrinkage, dynamic membrane blebbing, chromatin condensation, DNA laddering, loss of phospholipids asymmetry, low ATP levels, and mild calcium overload. This type of cell death normally occurs in penumbral region at the ischemic injury site and in different regions in various neurodegenerative diseases.
Phytochemicals Signal Transduction and Neurological Disorders Phytochemicals are heterogeneous group of bioactive compounds produced by plants, which are extensively researched by scientists for their health-promoting potentials in human diseases. Unlike vitamins and minerals, phytochemicals are not required for sustaining cell viability, but they play an important role in protecting tissues and cells from the harmful effects of oxidative stress and inflammation. Examples of phytochemicals include catechins, resveratrol, ginkgo biloba, curcumin, and sulfur compounds found in garlic. Although, the precise molecular mechanisms associated with beneficial effects of phytochemicals still remain the subject of intense investigations, but it is becoming increasingly evident that phytochemicals mediate their effects by counteracting, reducing, and repairing the damage caused by oxidative stress and neuroinflammation. In addition, phytochemicals also stimulate the synthesis of adaptive enzymes and proteins through the stimulation of a transcription factor called Nrf2 and induction of phase II detoxifying enzymes. Consumption of phytochemicals induces neurohormetic response that results in the expression of adaptive stress-resistance genes that are responsible for encoding antioxidant enzymes, protein chaperones, and neurotrophic factor (BDNF). Based on the stimulation of signal transduction network and adaptive stress-resistance genes, it is proposed that the use of phytochemicals from childhood to old age along with regular exercise is an important strategy for maintaining normal aging and delaying onset of age-related neurological disorders (stroke, Alzheimer disease, and Parkinson disease). Phytochemicals Signal Transduction and Neurological Disorders presents readers with cutting edge and comprehensive information not only on bioavailability, and mechanism of action of phytochemicals in the brain, but also provides the molecular mechanism associated with beneficial effects of phytochemicals in neurotraumatic (stroke, spinal cord trauma, and traumatic brain injury) and neurodegenerative (Alzheimers disease, Parkinson disease, Huntington disease, and amyotrophic lateral sclerosis) diseases.
This is the first book on the market that explores the importance of curcumin for the treatment of neurological disorders. It has been estimated that 35.6 million people globally had dementia in 2010 and the prevalence of dementia has been predicted to double every 20 years. Thus, 115.4 million people may be living with dementia in 2050. Alzheimer’s disease (AD) is the leading cause of dementia and is present in 60%–70% of people with dementia. Unless new discoveries are made in the prevention or treatment of AD, the number of cases in the US alone is estimated to increase threefold, to 13.2 million by the year 2050. Thus, it is important to focus on delaying and treating the onset of AD by curcumin may be an important step for controlling AD. Regular consumption of healthy diet containing curcumin enriched foods, moderate exercise, and regular sleep may produce beneficial effects not only on motor and cognitive functions, but also on memory deficits that occur to some extent during normal aging and to a large extent in AD. Delaying the onset and progression of AD and improving its symptoms by few years with regular consumption of curcumin may relieve some of the burden on health care systems. In service of this goal, this volume gives readers a comprehensive and cutting edge description of the importance of curcumin for the treatment of AD in cell culture and animal models in a manner that is useful not only to students and teachers but also to researchers, dietitians, nutritionists and physicians. It can be used as supplement text for a range of neuroscience and nutrition courses. Clinicians, neuroscientists, neurologists and pharmacologists will find this book useful for understanding molecular aspects of AD treatment by curcumin.
"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 occu"
