The Intersection of Osteoarthritis and Alzheimer’s: A Molecular Perspective

David Stone^*
*Correspondence: David Stone, Department of Internal Medicine, University of Sumatera Utara, Medan, Indonesia, Email:

Introduction

Osteoarthritis and Alzheimer’s disease are widespread age-related disorders that significantly affect the quality of life for millions of people globally. Although they affect different anatomical systems, emerging research has revealed compelling molecular links between these two conditions. This article delves into the shared pathways, mechanisms, and promising prospects that connect OA and AD. Both OA and AD are characterized by chronic inflammation. In OA, inflammation primarily stems from cartilage degradation and joint damage, while AD is driven by neuroinflammation, which is associated with the accumulation of amyloid-beta plaques and tau protein tangles. Common inflammatory mediators, such as cytokines (e.g., TNF-α, IL-1β) and chemokines, create a pro-inflammatory environment that accelerates the progression of both diseases. Additionally, oxidative stress plays a crucial role in the pathogenesis of both OA and AD. The production of Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) leads to cellular damage, worsening cartilage destruction in OA and neuronal dysfunction in AD [1].

Mitochondrial dysfunction, impaired antioxidant defense mechanisms and lipid peroxidation are shared consequences of oxidative stress, linking the two diseases mechanistically [2]. Autophagy, a cellular process responsible for degrading damaged organelles and proteins, is dysregulated in both OA and AD. Impaired autophagic flux contributes to the accumulation of protein aggregates, such as Aβ in AD and misfolded proteins in OA. Shared regulators of autophagy, including mTOR and AMPK signaling pathways, highlight common molecular pathways underlying disease pathology.

Description

Cellular senescence and apoptosis are key contributors to the progression of both OA and AD. In OA, senescent chondrocytes within the joints display altered secretory profiles, which promote inflammation and tissue degradation. Likewise, neuronal apoptosis and senescence are prominent in the brains of individuals with AD, contributing to cognitive decline [3]. Shared pathways involving p53, NF-KB and Bcl-2 family proteins contribute to cell fate decisions in both conditions. Identifying shared molecular pathways opens avenues for developing targeted therapies with broad applicability across OA and AD. Anti-inflammatory agents, antioxidants and modulators of autophagy represent promising candidates for disease-modifying interventions.

Multi-modal approaches targeting multiple pathways simultaneously may offer synergistic benefits in managing both conditions. Personalized medicine approaches leveraging genetic, epigenetic and biomarker data hold potential for stratifying patients based on disease severity, progression and treatment response. Precision targeting of specific molecular subtypes within OA and AD cohorts can optimize therapeutic outcomes while minimizing adverse effects. Drug repurposing presents a cost-effective strategy for accelerating therapeutic development in OA and AD [4]. Compounds with established safety profiles targeting shared pathways, such as NSAIDs, statins and autophagy modulators, can be repurposed for dual indication treatment, providing immediate clinical benefits to patients [5].

Conclusion

The complex interaction of shared molecular pathways highlights the unexpected connection between OA and AD. Understanding these common mechanisms opens up exciting possibilities for the development of novel therapies and the advancement of precision medicine. By adopting a comprehensive approach that targets the converging pathogenic processes, we can work towards more effective strategies for managing and preventing these debilitating age-related disorders.

Acknowledgement

None.

Conflict of Interest

None.

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