review · Naunyn-Schmiedeberg s Archives of Pharmacology
Neurodegenerative conditions such as Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis pose complex challenges due to their progressive nature and intricate biological pathways. A central feature across these conditions is mitochondrial dysfunction. Mitochondria are vital for neuronal health, overseeing key processes that include cellular energy generation, calcium signalling, cell death regulation, dynamics, and axonal transport, alongside interactions with other cellular components. Current scientific literature indicates a strategic shift away from merely treating symptoms towards developing innovative interventions focused on restoring mitochondrial integrity. By concentrating on mechanisms such as mitochondrial quality control and counteracting oxidative stress, researchers aim to preserve neuronal connections and integrity. Examining these pathways offers potential insights into novel therapies designed to address the underlying disease progression rather than temporary relief.
Neurodegenerative diseases remain notoriously difficult to treat, often leaving patients with limited options that address only outward symptoms. Understanding how cell energy centres break down opens doors to interventions that might slow or halt biological decay, potentially preserving cognitive and physical functions for longer.
The work indicates potential drug discovery opportunities for pharmaceutical developers seeking therapeutic targets in mitochondrial quality control and oxidative stress pathways. However, as a conceptual literature review exploring broad mechanisms rather than testing a specific compound or formulation, this research represents an early discovery phase that is distant from clinical and market deployment.
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Neurodegenerative disorders present significant challenges to modern medicine because of their complex etiology, pathogenesis, and progressive nature, which complicate practical treatment approaches. Mitochondrial dysfunction is an important contributor to the pathophysiology of various neurodegenerative illnesses, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). This review paper examines the current literature highlighting the multifaceted functions of mitochondria, including energy production, calcium signaling, apoptosis regulation, mitochondrial biogenesis, mitochondrial dynamics, axonal transport, endoplasmic reticulum-mitochondrial interactions, mitophagy, mitochondrial proteostasis, and their crucial involvement in neuronal health. The literature emphasizes the increasing recognition of mitochondrial dysfunction as a critical factor in the progression of neurodegenerative disorders, marking a shift from traditional symptom management to innovative mitochondrial-based therapies. By discussing mitochondrial mechanisms, including mitochondrial quality control (MQC) processes and the impact of oxidative stress, this review highlights the need for novel therapeutic strategies to restore mitochondrial function, protect neuronal connections and integrity, and slow disease progression. This comprehensive review aims to provide insights into potential interventions that could transform the treatment landscape for neurodegenerative diseases, addressing symptoms and underlying pathophysiological changes.
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DOI: 10.1007/s00210-025-04014-0
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