Targeting Molecular Pathways for Neuroprotection in Neurodegenerative Disorders

Abstract

Alzheimer's disease, Parkinson's disease and Huntington's disease are examples of neurodegenerative diseases that are typified by the progressive loss of neuronal structure and function. Recently, shared molecular and cellular mechanisms have connected neurodegenerative processes to migraine, a common neurological condition. Both disorders include neuroinflammation, mitochondrial dysfunction, oxidative stress and impaired calcium signalling all of which lead to damage to neurons and dysfunction. There are promising treatment approaches for migraine treatment and neuroprotection by focusing on certain molecular pathways. Promoting autophagy, improving mitochondrial function and modifying inflammatory cytokines have become important strategies for maintaining brain health. Mitigating neurodegeneration and migraine symptoms may also be achieved by preventing the development of reactive oxygen species (ROS) and cortical spreading depression. By creating customized medication delivery systems, nanotechnology advancements have improved the effectiveness and bioavailability of neuroprotective drugs. New research shows how crucial calcium channel modulation and synaptic maintenance are to the pathophysiology of migraines and neurodegenerative illnesses. This study highlights how molecular pathways in these disorders converge and highlights novel treatment approaches to fully address neuronal dysfunction. Knowing these interrelated pathways opens up new possibilities for integrative therapy strategies, which may help patients with neurodegenerative diseases as well as migraines.