Alzheimer DiseaseRobert D. Terry Lippincott Williams & Wilkins, 1999 - Broj stranica: 457 The Second Edition of this highly acclaimed volume examines every major aspect of Alzheimer disease -- clinical, epidemiologic, structural, chemical, genetic, molecular, and therapeutic. This edition includes expanded coverage of the cellular-level exploration of related dementing disorders, with in-depth presentation of prion diseases, Pick's disease, fronto-temporal disorders, transgenic models, and biochemistry of presenilins. Treatment of symptoms with therapeutic drugs is discussed, along with outcomes of and problems inherent in clinical trials for AD. The broad coverage of AD in this book benefits clinicians, educators, investigators, and health administrators. |
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Stranica 107
... increase in its degradation to B - amyloid . These events , in turn , could lead to the development of B - amyloid - containing diffuse plaques . Supporting this situ- ation , the brains of boxers with dementia pugilistica have been ...
... increase in its degradation to B - amyloid . These events , in turn , could lead to the development of B - amyloid - containing diffuse plaques . Supporting this situ- ation , the brains of boxers with dementia pugilistica have been ...
Stranica 406
... increased TBARS in the inferior temporal cortex ( 93 ) , whereas another found no significant difference in TBARS in the neocortex of AD subjects ( 94 ) . Others also reported an increase in lipid perox- idation in the temporal lobe in ...
... increased TBARS in the inferior temporal cortex ( 93 ) , whereas another found no significant difference in TBARS in the neocortex of AD subjects ( 94 ) . Others also reported an increase in lipid perox- idation in the temporal lobe in ...
Stranica 433
... increase associated with aging ( 132 ) . The increase in brain MAO - B may result in an increase in the oxidative deamina- tion of monoamines , with subsequent formation of hydrogen peroxide and other free radicals , resulting in lipid ...
... increase associated with aging ( 132 ) . The increase in brain MAO - B may result in an increase in the oxidative deamina- tion of monoamines , with subsequent formation of hydrogen peroxide and other free radicals , resulting in lipid ...
Sadržaj
Clinical Presentation | 6 |
Noncognitive Symptoms of Alzheimer Disease | 25 |
Neuropsychology of Alzheimer Disease | 39 |
Autorska prava | |
Broj ostalih dijelova koji nisu prikazani: 26
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Uobičajeni izrazi i fraze
abnormal Acad Sci USA activity allele Alzheimer disease Alzheimer's disease amyloid precursor protein Ann Neurol ApoE apolipoprotein apoptosis Arch Neurol areas Aẞ associated atrophy B-amyloid basal forebrain behavioral Biol Brain Res cells cerebral cortex cholinergic cholinergic neurons chromosome clinical cognitive impairment correlation cortical deficits degeneration demented density diagnosis disorders drug effects elderly entorhinal ethnic Exp Neurol familial frontal frontotemporal dementia function gene genetic growth factor hippocampus human immunoreactivity increased lesions levels Lewy body lobe Masliah memory mer's disease metabolism microglia monkeys mutations Natl Acad Sci neocortex neuritic Neurobiol Aging neurodegenerative neurofibrillary tangles neurofilament Neurology neuronal loss neurons neuropsychological Neurosci Neurosci Lett normal onset Parkinson disease pathological patients peptide phosphorylation presenilin prevalence Proc Natl Acad Prpsc Psychiatry receptor regions reported risk factors senile dementia senile plaques studies subcortical symptoms synaptic syndrome tau protein temporal tion transgenic mice trophic factors vascular dementia