The necessity for a deeper understanding of neurological diseases such as Alzheimer's disease (AD) that increase in frequency as a function of age has become of paramount importance with the coming of age of the baby boom generation as well as the increasing social demands for individuals to perform better and longer. AD is characterized by a gradual decline in cognitive function and presence of pathological inclusions such as Aβ plaques and neurofibrillary tangles composed of hyperphosphorylated tau in the brain. These are the main hallmarks of the disease and focus of most current therapeutic strategies. As such, the development of transgenic and nontransgenic models of AD over the last decade has primarily focused on these pathological markers. These models have become promising tools to decipher the mechanistic importance of tau phosphorylation and Aβ deposits, as well the relationship between each other, other pathological AD-related events, and cognitive loss. However, while seemingly obvious, it is important to remember that the validity of an animal model of disease is tightly linked to the ability of the animal to mimic the signs of the disease–which goes beyond the pathology and needs to include cognitive decline and neuronal loss. This special issue seeks to provide an updated and critical evaluation of the available animal models of AD with the primary goal to deepen our mechanistic understanding of AD and elucidate how the development of these models has led or can lead to novel therapies for AD patients.

We invite authors to present original research articles as well as review articles that will encourage the primary goals of this special issues. We are interested in manuscripts that focus on novel animal models (transgenic or nontransgenic) and novel therapeutic strategies tested in such mouse models. While the majority of the work is carried out in rodents, we also welcome manuscripts that focus on nonrodent models of AD.

The topics to be covered include, but are not limited to:

• Development of novel transgenic or nontransgenic animal models of AD (rodents or other)
• Mechanistic studies of AD-related pathology in animal models including, but not limited to, APP/Aβ and/or tau hyperphosphorylation (i.e., oxidative stress, mitochondrial, inflammatory, cell cycle changes etc.)
• Development of novel behavioral or translational methodologies to determine impairment in models of AD
• Novel therapeutic approaches to modulate AD pathology and cognitive impairment

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ijad/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable: