Abstract
Alzheimer's disease (AD) represents one neurodegenerative disorder whose etiology remains unknown. Animal model systems for AD are further hampered by the absence of the tools necessary to duplicate some of the known neurodegenerative changes. For example, slow progressive neurodegeneration has been difficult to reproduce. The studies presented in this chapter were conducted to determine whether the neurochemical deficits noted in AD could produce some of the cognitive symptoms of AD in animals, and whether the cognitive deficits so produced would be amenable to pharmacological alleviation. Based on these investigations, the chapter shows that some of the neurochemical deficits noted in AD may be intimately linked to another hallmark of the AD brain, namely, the synthesis of β-amyloid precursor protein.
Original language | English |
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Title of host publication | Brain and Memory |
Subtitle of host publication | Modulation and Mediation of Neuroplasticity |
Publisher | Oxford University Press |
ISBN (Electronic) | 9780199847877 |
ISBN (Print) | 9780195082944 |
DOIs | |
State | Published - 22 Mar 2012 |
Keywords
- Alzheimer's disease
- Animal model
- Cognitive deficits
- Neurochemical deficits
- Neurodegeneration
- β-amyloid precursor protein