# Role of mitochondria in neuronal function and survival in the enteric and central nervous systems

## TL;DR

This review explains how mitochondria are crucial for neuron health and how their dysfunction can lead to neurological diseases.

## Contribution

The paper integrates evidence from both central and enteric nervous systems to emphasize mitochondria's role in neurodegenerative diseases.

## Key findings

- Mitochondrial dysfunction contributes to neuronal cell loss through impaired bioenergetics and oxidative stress.
- Mitochondrial defects are linked to both primary and secondary neurological disorders like Alzheimer's and Parkinson's.
- Mitochondria are potential therapeutic targets for neurodegenerative diseases.

## Abstract

Mitochondria are indispensable organelles that not only generate cellular energy through oxidative phosphorylation but also regulate calcium homeostasis, redox balance, and apoptotic signaling. Given the high metabolic demands of neurons, mitochondrial function and resilience mechanisms are essential for neuronal development, maturation, and survival; when these systems fail, pathological outcomes can arise. This review highlights the critical role of mitochondria in maintaining neuronal function, with discussion related to both the central (CNS) and enteric (ENS) nervous systems. We present how mitochondrial dysfunction, through impaired bioenergetics, oxidative stress, defective quality control, and altered dynamics, can drive neuronal cell loss. Furthermore, we highlight the link between mitochondrial defects and nervous system pathological outcomes in both primary mitochondrial disorders, such as mitochondrial neurogastrointestinal encephalomyopathy, and secondary mitochondrial disorders, such as Alzheimer, Parkinson, and Huntington disease, as well as amyotrophic lateral sclerosis. By integrating evidence from the CNS and ENS, this review highlights the central role of mitochondria in supporting and preserving neuronal health, as well as the potential of mitochondria as therapeutic targets in neurodegenerative disease.