Exploring the Interplay Between Neuroinflammation, Mitochondrial Dysfunction, and Novel Therapeutic Targets in Alzheimer's Disease

Abstract:: Alzheimer's disease (AD) is the most common cause of dementia worldwide, affecting over 50 million people globally. Despite significant efforts to understand its underlying pathophysiology, effective disease-modifying treatments remain elusive. Research has increasingly focused on the molecular mechanisms contributing to AD progression, particularly the roles of neuroinflammation and mitochondrial dysfunction. Both have been implicated in disrupting neuronal homeostasis, exacerbating synaptic failure, and neuronal death. Neuroinflammation refers to the activation of the brain’s immune system in response to various insults, including amyloid-beta (Aβ) deposition. This immune response can, in turn, trigger mitochondrial dysfunction, leading to disrupted energy production and accelerated oxidative stress in neurons. These processes are closely intertwined, forming a feedback loop that worsens AD pathology. Targeting these mechanisms offers promising therapeutic strategies. Recent advances, including gene therapies, mitochondrial-targeted drugs, and immune-modulating agents, have opened new avenues for potentially halting or reversing AD progression.