Microglia in Alzheimer’s Disease
1Department of Pathology and Laboratory Medicine, University of California Davis Medical Center, Sacramento, CA 95817, USA
2Department of Pharmacology, Physiology & Therapeutics, University of North Dakota School of Medicine and Health Sciences, Grand Forks, ND 58203, USA
3Harvard Medical School, Neuroimmunology & Innate Immunity Lab., Center for Immunology & Inflammatory Diseases and Division of Infectious Diseases, Massachusetts General Hospital, Charlestown, MA 02129, USA
4Department of Neuroimmunology, Research Institute of Environmental Medicine, Nagoya University, Fucho-cho, Chikusa, Nagoya 464-8601, Japan
Microglia in Alzheimer’s Disease
Description
Alzheimer's disease (AD) is the major cause of dementia and one of the most disabling health conditions worldwide. Microglia, the major inflammatory cells in the brain, play a pivotal role in the initiation and progression of AD. Despite current advances in our understanding of AD, the role of microglia in AD remains mysterious—microglia are either neuroprotective or neurotoxic. It is likely that the role of microglia in AD is not simplistically good or bad; they respond to stimuli with an array of activation profiles that depend on the age of the individual, the kind of stimuli, and modulation by neurons and astrocytes. New insights into the complex actions of microglia in AD will aid the development of therapeutic approaches that “fine-tune” the microglial activation profile to our advantage.
We invite investigators to contribute original research articles as well as review articles that will stimulate the continuing efforts to understand the actions of microglia in AD. Technically, microglia are hard to study because they are small, less abundant, and less immunoreactive than other neural cells in vivo and invariably become activated and altered when processed ex vivo. Therefore, we are also interested in articles describing novel methods to explore microglia. Potential topics include, but are not limited to:
- Recent developments in microglial research techniques
- Microglial stimuli in AD
- Heterogeneity of microglial activation in AD
- Regulation of microglial chemotaxis and phagocytosis
- Role of microglial senescence/dystrophy in AD
- Mechanism of neurotoxicity by microglia (including mechanisms related to Aβ and tau)
- Therapeutic strategy targeting microglia (including clinical trials and epidemiological studies on anti-inflammatory reagents)
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: