**Alzheimer's Disease: From Animal Models to the Human Syndrome**

Erika Orta‐Salazar, Isaac Vargas‐Rodríguez, Susana A Castro‐Chavira, Alfredo I. Feria‐Velasco and Sofía Díaz‐Cintra

Additional information is available at the end of the chapter

http://dx.doi.org/10.5772/64619

#### **Abstract**

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190 Update on Dementia

Some animal models, genetically modified (such as murine) and sporadic (as others species), enable the study of the origin of specific lesions observed in human neurode‐ generative diseases. In particular, Alzheimer's disease (AD) models have been designed to test the hypothesis that certain lesions are associated with functional and morpho‐ logical changes beginning with memory loss and impairment in activities of daily life. This review compares and evaluates the phenotypes of different AD animal models, on the basis of the specific objectives of each study, with the purpose of encompassing their contributions to the comprehension of the AD signs and symptoms in humans. All these models contribute to the comprehension of the human AD mechanisms regarding the heterogeneity of AD phenotypes: the overlap between AD and age‐related changes, the variability of AD onset (early or late), the probable reactiveness of amyloid‐β and tau proteins, the scarcity of senile plaques and/or neurofibrillary tangles in some AD cases, the spatial correlation of the pathology and cerebral blood vessels, and the immuno‐ logical responses (microglial aging) and synaptopathy. Altogether, these considera‐ tions may contribute to find therapies to treat and prevent this disease.

**Keywords:** Alzheimer's disease, nutritional risk, murine, human, genetic Alzheimer's disease, sporadic Alzheimer's disease

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