Pharmacological Strategies for Modulating Mitochondrial Dysfunction in Neurodegenerative Disease

Abstract

Neurodegenerative diseases present a formidable challenge as they progressively compromise neuronal structures and functions. This paper explores the intricate landscape of neurodegenerative disorders, encompassing Alzheimer's, Parkinson's, Huntington's, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis. Mitochondria, acknowledged as cellular powerhouses, crucially maintain neural health by influencing energy production, calcium homeostasis, ROS regulation, apoptosis, metabolism, neurotransmitter synthesis, neuroplasticity, dynamics, and neuroprotection. Mitochondrial dysfunction emerges as a common denominator linking neurodegenerative diseases, affecting vital pathways like energy production, oxidative stress, apoptosis, DNA mutations, calcium dysregulation, mitophagy, and dynamics. The paper underscores the implications of mitochondrial dysfunction in diseases such as Alzheimer's, Parkinson's, Huntington's, and ALS. This paper underscores the importance of diagnostic biomarkers and envisions future prospects, including genetic therapies, mitochondrial replacement therapy, small molecule therapeutics, metabolic regulation, and diagnostic biomarkers. Acknowledging the complexity of mitochondrial dysfunction, ongoing research holds promise for advancing understanding, diagnosis, and treatment of neurodegenerative diseases. Regular updates are crucial for staying informed in this dynamic field of mitochondrial medicine. Thus we explore different recent advances to create a descriptive illustration of how modulation of neurodegenerative diseases can be done by help of mitochondrial changes.