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A New Link Between Arthritis and Alzheimer's Disease?
Author(s) -
Squire Michaela,
Alkhouli Mustafa F.,
Anderson Miranda,
Castro Monica,
AlNakkash Layla,
Broderick Tom L.,
Plochocki Jeffrey H.
Publication year - 2018
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2018.32.1_supplement.640.1
Subject(s) - inflammation , arthritis , medicine , cartilage , muscle hypertrophy , pathogenesis , chondrocyte , cognitive decline , inflammatory arthritis , pathology , immunology , disease , anatomy , dementia
Recently, systemic inflammation has been implicated in the pathogenesis of Alzheimer's disease (AD). This inflammation has the ability to exacerbate both motor and cognitive symptoms of the disease through increasing amounts of inflammatory markers like TNF‐α and C‐Reactive Protein, as well as amyloid plaque depositions within many areas throughout the body, including articular cartilage of synovial joints. These inflammatory markers and amyloid plaques are related to the development of arthritis. In fact, arthritis is a risk factor for cognitive impairment in the elderly. For this reason, we hypothesize inflammatory mediators associated with the development of AD may also affect articular cartilage metabolism, specifically hypertrophy‐like changes induced by chondrocyte activation by inflammatory cytokines. Here, we compare expression of type X collagen (col10a1), a standard marker for chondrocyte hypertrophy, in tibiofemoral joint articular cartilage of 7‐month‐old male wild type mice with mice of the 3xTg‐AD model for AD. Results show that expression of col10a1 in mice with the Alzheimer's phenotype is significantly reduced in comparison with the wild type mice ( P < 0.05). This reduction is consistent with inhibited col10a1 expression by chondrocytes identified in arthritic cartilage. Our exploratory study suggests neurodegenerative and arthritogenic changes identified in many AD patients may be linked to a common systemic inflammatory process, and warrants further investigation. This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .