Knee osteoarthritis accelerates amyloid beta deposition and neurodegeneration in a mouse model of Alzheimer's disease

Knee osteoarthritis (OA) is characterized by knee cartilage degeneration and secondary bone hyperplasia, resulting in pain, stiffness, and gait disturbance. The relationship between knee OA and neurodegenerative diseases is still unclear. This study used an Alzheimer's disease (AD) mouse model to observe whether osteoarthritis accelerates dementia progression by analyzing brain histology and neuroinflammation. Knee OA was induced by destabilizing the medial meniscus (DMM) in control (WT) and AD (5xFAD) mice before pathological symptoms. Mouse knee joints were scanned with a micro-CT scanner. A sham operation was used as control. Motor and cognitive abilities were tested after OA induction. Neurodegeneration, beta-amyloid plaque formation, and neuroinflammation were analyzed by immunostaining, Western blotting, and RT-PCR in brain tissues. Compared with sham controls, OA in AD mice increased inflammatory cytokine levels in brain tissues. Furthermore, OA significantly increased beta-amyloid deposition and neuronal loss in AD mice compared to sham controls. In conclusion, knee OA accelerated amyloid plaque deposition and neurodegeneration in AD-OA mice, suggesting that OA is a risk factor for AD.

Automated summary

This study investigated the relationship between knee osteoarthritis (OA) and Alzheimer's disease (AD) by using an AD mouse model. The researchers induced knee OA in control and AD mice and analyzed the effects on brain histology and neuroinflammation. The results showed that OA increased inflammatory cytokine levels, beta-amyloid plaque deposition, and neuronal loss in AD mice, suggesting that knee OA could accelerate dementia progression in AD.