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 296
... Aẞ formation . Indeed , stimulation of protein kinase C by phorbol esters in primary human neurons increases APP , -a secretion without decreasing the secretion of Aẞ ( 37 ) M . THE GENERATION OF AMYLOID ẞ - PROTEIN Even before the a ...
... Aẞ formation . Indeed , stimulation of protein kinase C by phorbol esters in primary human neurons increases APP , -a secretion without decreasing the secretion of Aẞ ( 37 ) M . THE GENERATION OF AMYLOID ẞ - PROTEIN Even before the a ...
Stranica 298
... Aẞ fragment . It appears that only after excessive cerebral accumulation of Aẞ peptides and the subsequent occurrence of multiple molecular and cellular changes do symptoms of dementia appear . One important line of support for this ...
... Aẞ fragment . It appears that only after excessive cerebral accumulation of Aẞ peptides and the subsequent occurrence of multiple molecular and cellular changes do symptoms of dementia appear . One important line of support for this ...
Stranica 300
... Aẞ region , one can conclude that deletion of APP , with its unique Aẞ sequence , has no critical consequences for mice . On the other hand , rodents in general appear not to convert as many of their APP molecules to Aẞ peptides ...
... Aẞ region , one can conclude that deletion of APP , with its unique Aẞ sequence , has no critical consequences for mice . On the other hand , rodents in general appear not to convert as many of their APP molecules to Aẞ peptides ...
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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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