More than half of all patients with diabetes develop neuropathic disorders affecting the distal sensory and/or motor nerves, or autonomic or cranial nerve functions. Glycemic control can decrease the incidence of neuropathy but is not adequate alone to prevent or treat the disease. This chapter introduces diabetic neuropathy with a morphological description of the disease then describes our current understanding of metabolic and molecular mechanisms that contribute to neurovascular dysfunctions. Key mechanisms include glucose and lipid imbalances and insulin resistance that are interconnected via oxidative stress, inflammation, and altered gene expression. These complex interactions should be considered for the development of new treatment strategies against the onset or progression of neuropathy. Advances in understanding the combined metabolic stressors and the novel study of epigenetics suggest new therapeutic targets to combat this morbid and intractable disease affecting millions of patients with type 1 or type 2 diabetes.
Many infectious agents, such as viruses, bacteria, and parasites, can cause inflammation of the central nervous system (CNS). Encephalitis is an inflammation of the brain parenchyma, which may result in a more advanced and serious disease meningoencephalitis. To establish accurate diagnosis and develop effective vaccines and drugs to overcome this disease, it is important to understand and elucidate the mechanism of its pathogenesis. This book, which is divided into four sections, provides comprehensive commentaries on encephalitis. The first section (6 chapters) covers diagnosis and clinical symptoms of encephalitis with some neurological disorders. The second section (5 chapters) reviews some virus infections with the outlines of inflammatory and chemokine responses. The third section (7 chapters) deals with the non-viral causative agents of encephalitis. The last section (4 chapters) discusses the experimental model of encephalitis. The different chapters of this book provide valuable and important information not only to the researchers, but also to the physician and health care workers.
Many infectious agents, such as viruses, bacteria, and parasites, can cause inflammation of the central nervous system (CNS). Encephalitis is an inflammation of the brain parenchyma, which may result in a more advanced and serious disease meningoencephalitis. To establish accurate diagnosis and develop effective vaccines and drugs to overcome this disease, it is important to understand and elucidate the mechanism of its pathogenesis. This book, which is divided into four sections, provides comprehensive commentaries on encephalitis. The first section (6 chapters) covers diagnosis and clinical symptoms of encephalitis with some neurological disorders. The second section (5 chapters) reviews some virus infections with the outlines of inflammatory and chemokine responses. The third section (7 chapters) deals with the non-viral causative agents of encephalitis. The last section (4 chapters) discusses the experimental model of encephalitis. The different chapters of this book provide valuable and important information not only to the researchers, but also to the physician and health care workers.
More than half of all patients with diabetes develop neuropathic disorders affecting the distal sensory and/or motor nerves, or autonomic or cranial nerve functions. Glycemic control can decrease the incidence of neuropathy but is not adequate alone to prevent or treat the disease. This chapter introduces diabetic neuropathy with a morphological description of the disease then describes our current understanding of metabolic and molecular mechanisms that contribute to neurovascular dysfunctions. Key mechanisms include glucose and lipid imbalances and insulin resistance that are interconnected via oxidative stress, inflammation, and altered gene expression. These complex interactions should be considered for the development of new treatment strategies against the onset or progression of neuropathy. Advances in understanding the combined metabolic stressors and the novel study of epigenetics suggest new therapeutic targets to combat this morbid and intractable disease affecting millions of patients with type 1 or type 2 diabetes.
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