Research Progress in Alzheimer's Disease and Dementia, Volumen1

Portada
Nova Publishers, 2007 - 462 páginas
Alzheimer's disease (AD) is the most common type of neurodegenerative disorder in the ageing population, with dementia as a common consequence. AD is defined pathologically by the appearance of extracellular senile plaques and intracellular neurofibrillary tangles, as described by Alois Alzheimer about a century ago. The causes for AD include genetic predisposition in a small population, ageing and environmental stresses in majority cases. The underlying pathogenic cascades, increases in expression of amyloid precursor protein and accumulation of Aß and reactive oxidant activity and inflammation, have the features of both adaptive, at least initially, and harmful when becoming excessive. Dementia, on the other hand, is a clinical diagnosis and is defined as globally, persistently impaired cognitive skills including memory. Alzheimer dementia refers to clinical dementia in patients who also have Alzheimer neuropathology. Alzheimer dementia is what brings the patients to seek medical treatments. An extraordinary inability to form new memory, especially of those episodic type, and executive dysfunction are among the earliest symptoms in AD patients. In end-stage AD, cognitive degeneration extends far beyond memory loss. The underlying causes include decreases in impaired brain metabolism, which results in impaired synaptic functions and capacities, thus impaired information processing, and eventually leads to neuronal injury and death. This book presents leading-edge research in this dynamic field.
 

Contenido

Neuroimaging in Alzheimers Disease and Mild Cognitive Impairment
1
Executive Dysfunction in Alzheimers Disease
25
Alzheimers Disease Therapies Updates on Genetic and Pharmacological Manipulations of 𝛃Secretase
39
Neuronal Deregulation of Tau Phosphorylation Implications for Mechanisms and Treatment of Alzheimers Disease
61
Immunotherapeutic Approach in Alzheimers Disease
79
Immunotherapy for Alzheimers Disease and Dementia
97
A𝛃Degrading Enzyme Neprilyusin
111
Memantine as an Antidementic Drug
147
Apolipoprotein E and Cerebral Amyloid Angiopathy in Alzheimers Disease
257
Limbic Metabolic Changes and Alzheimers Disease
285
Oxidative Damage is the Earliest Change of Alzheimers Disease Therapeutic Opportunities
301
Chronic Antioxidant Treatments and Memory in a Transgenic Mouse Model of Alzheimers Disease
319
Drosophila as a Model for Studying Disease Mechanisms of Alzheimers and Related Dementia
343
Androgens ApoE and Alzheimers Disease
361
Pivotal Roles of Cholesterol and Gangliosides in Aggregation of Amyloid 𝛃Protein
389
Imaging Cerebral Atrophy in Alzheimers Disease
403

Neurogenesis and Alzheimers Disease
177
Gloxalase I and Its Role in Human Disease
191
Brain Insulin Function and Insulin Signal Transduction in Sporadic Alzheimers Disease
205
Contributors
437
Index
441
Derechos de autor

Términos y frases comunes

Pasajes populares

Página 431 - Report of the Quality Standards Subcommittee of the American Academy of Neurology.

Acerca del autor (2007)

Miao-Kun Sun, Ph.D. obtained his Ph.D. at the Department of Pharmacology, University of Virginia, in 1986, and continued postdoctoral research at the same department for two more years. After a brief research period (one year) at the Department of Physiology, Royal Free Hospital School of Medicine, University College of London, he accepted a faculty position at Department of Neurology and Neuroscience, Cornell University Medical College in New York in 1990. His current position is Professor at Blänchette Rockefeller Neurosciences Institute (holding the same position since 2000).

Información bibliográfica