Increasing basic science and clinical evidence implicates inflammatory processes that result in glial activation in the pathogenesis of Alzheimer's disease. Immunohistochemical studies have shown that the plaques and tangles of AD are heavily infiltrated with activated glial cells, in addition to inflammatory factors, such as cytokines, chemokines, complement components, and acute phase proteins that colocalize as secondary components in senile plaques or are overproduced in AD brains. The importance of inflammation in AD is affirmed by data showing polymorphisms in cytokines and other immune molecules in people afflicted with AD, and epidemiological studies indicate that nonsteroidal anti-inflammatory drugs (NSAIDs) diminish the risk of developing AD. Activation of inflammatory pathways early or preceding the disease would provide support for a causative role for inflammation; although inflammation could still be a key driving force and accelerate AD progression if activated at a later stage of the disease.

We invite authors to contribute original research articles as well as review articles that stimulate the continuous effort to define the role of inflammation in AD as well as provide a more complete risk assessment, therefore, allowing a new approach for prevention, treatment, and interventions to retard disease progression.

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

• Cholinergic anti-inflammatory signalling
• Peripheral inflammatory biomarkers in AD
• Immunotherapy in the treatment of AD
• Why block inflammation in AD?
• Genetic basis of a specific inflammatory disease: Alzheimer's disease
• Neuroinflammation and cognitive functions in CNS diseases

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: