Lessons from Microglia Aging for the Link between Inflammatory Bone Disorders and Alzheimer's Disease

Hiro Take, Hiroshi Nakanishi

Research output: Contribution to journalReview article

8 Citations (Scopus)

Abstract

Bone is sensitive to overactive immune responses, which initiate the onset of inflammatory bone disorders, such as rheumatoid arthritis and periodontitis, resulting in a significant systemic inflammatory response. On the other hand, neuroinflammation is strongly implicated in Alzheimer's disease (AD), which can be enhanced by systemic inflammation, such as that due to cardiovascular disease and diabetes. There is growing clinical evidence supporting the concept that rheumatoid arthritis and periodontitis are positively linked to AD, suggesting that inflammatory bone disorders are risk factors for this condition. Recent studies have suggested that leptomeningeal cells play an important role in transducing systemic inflammatory signals to brain-resident microglia. More importantly, senescent-type, but not juvenile-type, microglia provoke neuroinflammation in response to systemic inflammation. Because the prevalence of rheumatoid arthritis and periodontitis increases with age, inflammatory bone disorders may be significant sources of covert systemic inflammation among elderly people. The present review article highlights our current understanding of the link between inflammatory bone disorders and AD with a special focus on microglia aging.

Original languageEnglish
Article number471342
JournalJournal of Immunology Research
Volume2015
DOIs
Publication statusPublished - Jan 1 2015

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Bone Diseases
Microglia
Periodontitis
Alzheimer Disease
Bone and Bones
Rheumatoid Arthritis
Inflammation
Cardiovascular Diseases
Brain

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

Cite this

Lessons from Microglia Aging for the Link between Inflammatory Bone Disorders and Alzheimer's Disease. / Take, Hiro; Nakanishi, Hiroshi.

In: Journal of Immunology Research, Vol. 2015, 471342, 01.01.2015.

Research output: Contribution to journalReview article

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