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Summary
Alzheimer's disease (AD) is a devastating age-related neurodegenerative disorder and the most frequent cause of senile dementia. The appearance of cognitive decline in this disease is associated with synaptic and neuronal loss, intracellular neurofibrillary tangles, the accumulation of intracellular and extracellular plaques of misfolded amyloid-β (Aβ) peptide, and local neuroinflammation. The major focus in AD therapeutics has been to directly target specific factors in the brain that are believed to be associated with pathogenesis—primarily Ab and tau proteins—by using immunological or pharmacological tools. However, in the clinic, these therapies have not shown efficacy in restoring cognitive function nor in arresting the disease course. In addition, treating brain inflammation, which often accompanies neurodegenerative diseases, with nonsteroidal anti-inflammatory drugs has shown limited or no effect on disease progression (1). Collectively, these results have led investigators to revisit the identification of the factors participating in AD and in particular the role of the immune system, including the resident brain myeloid cells (microglia) and the innate and adaptive arms of the immune system.
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