Molecular Mechanisms Linking Osteoarthritis and Alzheimer's Disease: Shared Pathways, Mechanisms and Breakthrough Prospects

Molecular Mechanisms Linking Osteoarthritis and Alzheimer's Disease: Shared Pathways, Mechanisms and Breakthrough Prospects

6 March 2024 | Idiongo Okon Umoh, Helton Jose dos Reis and Antonio Carlos Pinheiro de Oliveira
This review explores the molecular mechanisms linking osteoarthritis (OA) and Alzheimer's disease (AD), highlighting shared pathways and potential therapeutic strategies. Both diseases are age-related and involve chronic low-grade inflammation, with OA contributing to systemic inflammation that may exacerbate AD pathogenesis. OA is characterized by joint cartilage degradation, synovitis, and subchondral bone changes, while AD is marked by neurodegeneration, amyloid-beta (Aβ) plaques, and hyperphosphorylated tau (tau) protein. Shared mechanisms include neuroinflammation, Aβ accumulation, tau pathology, and dysregulated microRNAs. OA can induce peripheral and brain inflammation, leading to increased Aβ deposition and neuroinflammation, which worsen AD. Genetic factors, such as APOE-ε4, play a role in both diseases. Environmental factors like obesity, diet, and pollution also contribute to both conditions. Research suggests that targeting inflammation, using disease-modifying drugs, and exploring precision medicine could offer new therapeutic approaches for both OA and AD. The review emphasizes the importance of understanding the complex interplay between these diseases to develop effective prevention and treatment strategies.This review explores the molecular mechanisms linking osteoarthritis (OA) and Alzheimer's disease (AD), highlighting shared pathways and potential therapeutic strategies. Both diseases are age-related and involve chronic low-grade inflammation, with OA contributing to systemic inflammation that may exacerbate AD pathogenesis. OA is characterized by joint cartilage degradation, synovitis, and subchondral bone changes, while AD is marked by neurodegeneration, amyloid-beta (Aβ) plaques, and hyperphosphorylated tau (tau) protein. Shared mechanisms include neuroinflammation, Aβ accumulation, tau pathology, and dysregulated microRNAs. OA can induce peripheral and brain inflammation, leading to increased Aβ deposition and neuroinflammation, which worsen AD. Genetic factors, such as APOE-ε4, play a role in both diseases. Environmental factors like obesity, diet, and pollution also contribute to both conditions. Research suggests that targeting inflammation, using disease-modifying drugs, and exploring precision medicine could offer new therapeutic approaches for both OA and AD. The review emphasizes the importance of understanding the complex interplay between these diseases to develop effective prevention and treatment strategies.
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