Abstract
Alzheimer's disease (AD) is the most common type of dementia. The pathological characterizations of AD are the depositions of a peptide called amyloid beta and of hyper phosphorylated tau protein, gliosis, and neuronal death. While less than 5% of AD cases are caused by genetic mutations, these mutations are the basis for the majority of the animal models of AD. Although not presenting the entire spectrum of AD symptoms, these animal models extend and deepen our understanding on the pathological processes in AD and the possible therapeutic interventions. Nevertheless, many of these therapeutic applications fail later in clinical trials. Understanding the advantages and limitations of AD animal models is crucial for future therapeutic interventions.
Original language | English |
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Title of host publication | Neuroprotection in Alzheimer's Disease |
Publisher | Elsevier Inc. |
Pages | 31-58 |
Number of pages | 28 |
ISBN (Electronic) | 9780128037126 |
ISBN (Print) | 9780128036907 |
DOIs | |
State | Published - 20 Jan 2017 |
Keywords
- A?
- APP
- Alzheimer's disease
- ApoE
- Inflammation
- Tau
- Transgenic models