Frontiers in Alzheimer's Disease Research

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Nova 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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Ausgewählte Seiten

Inhalt

Inflammatory Oxidative and Vascular Factors Affecting Neuronal Cell Death in Alzheimers Disease
1
Neuronal Cell Death in Alzheimers Disease and its Potential Therapy with Neuroprotective Factors
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
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Beliebte Passagen

Seite 138 - Report of the Quality Standards Subcommittee of the American Academy of Neurology.
Seite 28 - R. (1991) Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment.
Seite 27 - Lewis, J., Dickson, DW, Lin, WL, Chisholm, L., Corral, A., Jones, G., Yen, S. H., Sahara, N., Skipper, L., Yager, D., Eckman, C., Hardy, J., Hutton, M., and McGowan, E.
Seite 34 - Excess brain protein oxidation and enzyme dysfunction in normal aging and in Alzheimer disease.
Seite 118 - Games, D; Adams, D; Alessandrini, R; Barbour, R; Berthelette, P; Blackwell, C; Carr, T; Clemens, J; Donaldson, T; Gillespie, F...
Seite 38 - Morgan, D., Diamond, DM, Gottschall, PE, Ugen, KE, Dickey, C., Hardy, J., Duff, K., Jantzen. P., DiCarlo, G., Wilcock, D., Connor, K., Hatcher, J., Hope, C.. Gordon, M...
Seite 93 - Storkebaum, E., Lambrechts, D., Dewerchin, M., Moreno-Murciano, MP, Appelmans, S., Oh, H., Van Damme, P., Rutten, B., Man, WY, De Mol, M., Wyns, S., Manka, D., Vermeulen, K., Van Den Bosch, L., Mertens, N., Schmitz, C., Robberecht, W., Conway, EM, Collen, D., Moons, L., and Carmeliet, P.
Seite 30 - K. (1991). Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease.
Seite 50 - Rigat B, Hubert C, Alhenc-Gelas F, Cambien F, Corvol P, Soubrier F. An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. J Clin Invest 1990;86: 1343- 1346.
Seite 42 - Eliasson MJ, Sampei K, Mandir AS, Hum PD, Traystman RJ, Bao J, Pieper A, Wang ZQ, Dawson TM, Snyder SH, Dawson VL (1997) Poly(ADP-ribose) polymerase gene disruption renders mice resistant to cerebral ischemia.

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