Frontiers in Alzheimer's Disease ResearchNova Publishers, 2006 - 353 Seiten Dementia is a brain disorder that seriously affects a person's ability to carry out daily activities. The most common form of dementia among older people is Alzheimer's Disease (AD), which involves the parts of the brain that control memory, thought and language. Age is the most important known risk factor for AD. The number of people with the disease doubles every 5 years beyond age 65. AD is a slow disease, starting with mild memory loss and ending with severe brain damage. The course the disease takes and how fast changes occur vary from person to person. On average, AD patients live from 8 to 10 years after they are diagnosed, though the disease can last for as many as 20 years. Current research is aimed at understanding why AD occurs and who is at greatest risk for developing it, improving the accuracy of diagnosis and ability to identify who is at risk, developing, discovering and testing new treatments for behavioural problems in patients with AD. This book gathers state-of-the-art research from leading scientists throughout the world which offers important information on understanding the underlying causes and discovering the most effective treatments for Alzheimer's Disease. |
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Seite 10
... transgenic mice are immunized with Aẞ a marked reduction in plaque deposition occurs [ 160 ] and is paralleled by protection from deficits in learning and memory [ 161 ] . Despite this compelling evidence for the toxicity of Aẞ the ...
... transgenic mice are immunized with Aẞ a marked reduction in plaque deposition occurs [ 160 ] and is paralleled by protection from deficits in learning and memory [ 161 ] . Despite this compelling evidence for the toxicity of Aẞ the ...
Seite 14
... transgenic AD mouse model showed that vitamin E supplementation reduced AP levels and amyloid deposition only in young mice [ 200 ] . This observation points to the importance of implementing preventative measures early in life , and is ...
... transgenic AD mouse model showed that vitamin E supplementation reduced AP levels and amyloid deposition only in young mice [ 200 ] . This observation points to the importance of implementing preventative measures early in life , and is ...
Seite 18
... transgenic mouse model of AD [ 300 ] . In addition to the various pathways of AP efflux from the brain , the receptor for advanced glycation end products ( RAGE ) also transports plasma AP across the blood brain barrier in a mouse model ...
... transgenic mouse model of AD [ 300 ] . In addition to the various pathways of AP efflux from the brain , the receptor for advanced glycation end products ( RAGE ) also transports plasma AP across the blood brain barrier in a mouse model ...
Seite 27
... transgenic mice expressing mutant tau and APP . Science , 293 , 1487-1491 . [ 6 ] Neve , R. L. , McPhie , D. L. , and Chen , Y. ( 2000 ) . Alzheimer's disease : a dysfunction of the amyloid precursor protein ( 1 ) . Brain Res , 886 , 54 ...
... transgenic mice expressing mutant tau and APP . Science , 293 , 1487-1491 . [ 6 ] Neve , R. L. , McPhie , D. L. , and Chen , Y. ( 2000 ) . Alzheimer's disease : a dysfunction of the amyloid precursor protein ( 1 ) . Brain Res , 886 , 54 ...
Seite 30
... transgenic mice and in Alzheimer's disease . Nature , 389 , 603-606 . [ 55 ] van der Wal , E. A. , Gomez - Pinilla , F. , and Cotman , C. W. ( 1993 ) . Transforming growth factor - beta 1 is in plaques in Alzheimer and Down pathologies ...
... transgenic mice and in Alzheimer's disease . Nature , 389 , 603-606 . [ 55 ] van der Wal , E. A. , Gomez - Pinilla , F. , and Cotman , C. W. ( 1993 ) . Transforming growth factor - beta 1 is in plaques in Alzheimer and Down pathologies ...
Inhalt
1 | |
55 | |
Synapse and Neuron Loss in Transgenic Mouse Models of Alzheimers Disease | 97 |
Neuropsychological Manifestations in Preclinical Alzheimers Disease | 127 |
Altered Brain Activation During Cognitive Process in Alzheimers Disease | 145 |
Premature Centromere Division PCD of the X Chromosome as a BioMarker of the Brain Cells reEntry Into the Cell Division Cycle in Alzheimers Dise... | 163 |
The Aging Brain The Risk Factor for Sporadic Alzheimers Disease SAD Cellular and Molecular Aspects | 179 |
Remembering Emotional Information Effects of Aging and Alzheimers Disease | 213 |
ApoE Anxiety and Alzheimers Disease | 227 |
Insulin Resistance Depressive Disorders and Alzheimers Disease | 251 |
Searching for Genetic Risk Factors in AD A NeverEnding Story | 279 |
APOE and Cognitive Function in Nondemented Old Age A Genetic Basis for Brain or Cognitive Reserve? | 309 |
Index | 333 |
Häufige Begriffe und Wortgruppen
acid activity age-related allele Alzheimer disease amygdala amyloid precursor protein Apoe mice apoE4 apolipoprotein apoptosis associated beta-amyloid Biol Brain Res caspase centromere cerebral Chem cholesterol chromosome clinical cognitive decline cognitive function cognitive reserve correlation cortex cortical cytotoxic dementia depressive disorders diabetes dysfunction effects emotional memory enzyme evidence expression extracellular Aẞ aggregates frontal gene genetic genotype glucose metabolism Hashimoto hippocampal human Humanin hypothesis increased induced inhibition insulin receptor Kensinger kinase late-onset levels measures of anxiety mechanisms mediated mild cognitive impairment MMSE molecular mouse model mutant Natl Acad Sci Neurobiol Aging Neurochem neurodegeneration neurofibrillary tangles Neurology neuron loss neuronal neuronal cell death neuronal death neuroprotective neuropsychological Neurosci Neurosci Lett neurotoxicity Niikura Nishimoto onset oxidative stress pathogenesis pathology pathway peptide polymorphism preclinical presenilin Psychiatry regulation risk factor role Selkoe signal SIPB sporadic ẞ-amyloid studies synapse transgenic transgenic mice vascular wild-type X chromosome
Beliebte Passagen
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