Research Progress in Alzheimer's Disease and Dementia, Volumen1Nova 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
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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 |
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Términos y frases comunes
Acad Sci USA acid activity aggregation allele Alzheimer Alzheimer's disease amyloid plaques amyloid precursor protein amyloid-ẞ antibodies APOE apolipoprotein Aẞ deposition associated atrophy BACE1 binding Biochem Biol Chem Brain Res CDK5 cells cellular cerebral amyloid angiopathy cholesterol cholinergic clearance clinical correlated cortical decreased deficits degradation dementia effects entorhinal cortex enzyme executive dysfunction expression extracellular factor formation frontal function gene genetic Ginkgo biloba Ginkgo biloba extract glucose glutamate hippocampal Hoyer human imaging immunization increased inhibition inhibitors insulin receptor learning and memory Lett memantine membrane metabolism mild cognitive impairment mouse model mutations Natl Acad Sci neprilysin Neurochem neurodegeneration neurofibrillary tangles neurogenesis Neurology neuronal Neurosci neurotoxicity NMDA receptor overexpression oxidative stress pathology patients peptide phosphorylation presenilin Proc Natl Acad protein kinase reduced regions role Selkoe DJ soluble spatial learning sporadic Alzheimer's disease ẞ-amyloid studies synaptic tau protein therapeutic toxicity transgenic transgenic mice treatment vitro vivo y-secretase
Pasajes populares
Página 431 - Report of the Quality Standards Subcommittee of the American Academy of Neurology.