5th Edition of International Neurology Conference 2026

Abstract

Neurodegenerative disorders represent a major global health challenge, characterized by progressive neuronal dysfunction and irreversible loss of neural networks. Diseases such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis share several pathological mechanisms, among which mitochondrial dysfunction has emerged as a central and unifying factor. Mitochondria play a critical role in neuronal survival by regulating cellular energy production, calcium homeostasis, oxidative stress responses, and apoptotic signaling. Given the exceptionally high metabolic demand of neurons, even subtle impairments in mitochondrial function can lead to significant neuronal vulnerability and degeneration.

Recent advances in neuroscience have highlighted how mitochondrial abnormalities contribute to neurodegenerative disease progression. Defects in mitochondrial dynamics including impaired fission and fusion processes can disrupt neuronal energy balance and accelerate the accumulation of toxic proteins such as amyloid-beta, tau, and alpha-synuclein. In addition, mitochondrial DNA mutations, oxidative stress, and disrupted bioenergetics have been linked to synaptic dysfunction and neuronal death across multiple neurodegenerative conditions.

This presentation examines the emerging role of mitochondrial dysfunction in the pathogenesis of neurodegenerative disorders and discusses how these insights may lead to new diagnostic and therapeutic strategies. Particular attention is given to recent discoveries regarding mitochondrial quality control mechanisms, including mitophagy and mitochondrial biogenesis, which play crucial roles in maintaining neuronal health. Furthermore, advances in molecular neuroscience and biomarker research are enabling the identification of mitochondrial signatures associated with early neurodegeneration.

Understanding mitochondrial involvement in neurodegenerative diseases may open new avenues for targeted therapies aimed at restoring neuronal bioenergetics and reducing oxidative stress. Therapeutic approaches under investigation include mitochondrial protective agents, metabolic modulators, and gene-based strategies designed to improve mitochondrial resilience. By exploring mitochondrial dysfunction as a shared pathological pathway, this work highlights its potential as a critical target for future neurodegenerative disease research and therapeutic development.