期刊
EXPERIMENTAL GERONTOLOGY
卷 107, 期 -, 页码 59-66出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.exger.2017.12.019
关键词
Peripheral innate immune system; Alzheimer disease; Microglia; Infections; Amyloid beta; Blood brain barrier; Neutrophils; NK cells
资金
- Canadian Institutes of Health Research (CIHR) [106634]
- Societe des medecins de l'Universite de Sherbrooke
- Research Center on Aging of the CIUSSS-CHUS, Sherbrooke
- Polish Ministry of Science and Higher Education statutory grant [02-0058/07/262]
- Agency for Science Technology and Research (A*STAR)
Alzheimer's disease is one of the most devastating neurodegenerative diseases. The exact cause of the disease is still not known although many scientists believe in the beta amyloid hypothesis which states that the accumulation of the amyloid peptide beta (A beta) in brain is the initial cause which consequently leads to pathological neuroinflammation. However, it was recently shown that A beta may have an important role in defending the brain against infections. Thus, the balance between positive and negative impact of A beta may determine disease progression. Microglia in the brain are innate immune cells, and brain-initiated inflammatory responses reflected in the periphery suggests that Alzheimer's disease is to some extent also a systemic inflammatory disease. Greater permeability of the blood brain barrier facilitates the transport of peripheral immune cells to the brain and vice versa so that a vicious circle originating on the periphery may contribute to the development of overt clinical AD. Persistent inflammatory challenges by pathogens in the periphery, increasing with age, may also contribute to the central propagation of the pathological changes seen clinically. Therefore, the activation status of peripheral innate immune cells may represent an early biomarker of the upcoming impact on the brain. The modulation of these cells may thus become a useful mechanism for modifying disease progression.
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