Mitochondrial Dysfunction in Neurodegeneration: A Translational Perspective

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 25 August 2025 | Viewed by 2291

Special Issue Editor


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Guest Editor
Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, KY 405036, USA
Interests: mitochondrial dysfunction after traumatic brain injury; mitochondrial bioenergetics

Special Issue Information

Dear Colleagues,

Mitochondria after traumatic brain injury (TBI) have emerged as a focal point in translational research, with their pivotal role in the pathophysiology of TBI being demonstrated. These cellular powerhouses play a multifaceted role in energy production, calcium homeostasis, and cell survival, making them susceptible to dysfunction following TBI.

Studies have revealed that TBI triggers a cascade of events leading to mitochondrial dysfunction. The disruption of mitochondrial membrane potential, impaired oxidative phosphorylation, and excessive reactive oxygen species (ROS) production contribute to energy depletion and oxidative stress, exacerbating neuronal damage. Mitochondrial DNA damage and altered mitochondrial dynamics further exacerbate the dysfunction, leading to a vicious cycle of neuronal death and inflammation.

Furthermore, understanding the intricate interplay between mitochondrial dysfunction and other secondary injury mechanisms, such as neuroinflammation and excitotoxicity, is crucial for developing comprehensive therapeutic strategies. Mitochondria serve as a convergence point for various pathways involved in TBI pathology, making them an attractive target for translational research.

This Special Issue aims to address the current trend in translational research, focusing on mitochondrial dysfunction after TBI by unraveling the underlying mechanisms and exploring potential therapeutic interventions as well as addressing technological advancements in the field, with the hope of ultimately improving outcomes and advancing clinical management in TBI patients.

Dr. Hemendra Vekaria
Guest Editor

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Keywords

  • mitochondrial dysfunction
  • traumatic brain injury
  • secondary damage
  • bioenergetics

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Published Papers (1 paper)

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Review

20 pages, 1096 KiB  
Review
Mitochondrial Alterations, Oxidative Stress, and Therapeutic Implications in Alzheimer’s Disease: A Narrative Review
by Erica Spina, Riccardo Rocco Ferrari, Elisa Pellegrini, Mauro Colombo, Tino Emanuele Poloni, Antonio Guaita and Annalisa Davin
Cells 2025, 14(3), 229; https://doi.org/10.3390/cells14030229 - 6 Feb 2025
Viewed by 1707
Abstract
The relationship between aging, mitochondrial dysfunction, neurodegeneration, and the onset of Alzheimer’s disease (AD) is a complex area of study. Aging is the primary risk factor for AD, and it is associated with a decline in mitochondrial function. This mitochondrial dysfunction is believed [...] Read more.
The relationship between aging, mitochondrial dysfunction, neurodegeneration, and the onset of Alzheimer’s disease (AD) is a complex area of study. Aging is the primary risk factor for AD, and it is associated with a decline in mitochondrial function. This mitochondrial dysfunction is believed to contribute to the neurodegenerative processes observed in AD. Neurodegeneration in AD is characterized by the progressive loss of synapses and neurons, particularly in regions of the brain involved in memory and cognition. It is hypothesized that mitochondrial dysfunction plays a pivotal role by disrupting cellular energy metabolism and increasing the production of reactive oxygen species (ROS), which can damage cellular components and exacerbate neuronal loss. Despite extensive research, the precise molecular pathways linking mitochondrial dysfunction to AD pathology are not fully understood. Various hypotheses have been proposed, including the mitochondrial cascade hypothesis, which suggests that mitochondrial dysfunction is an early event in AD pathogenesis that triggers a cascade of cellular events leading to neurodegeneration. With this narrative review, we aim to summarize some specific issues in the literature on mitochondria and their involvement in AD onset, with a focus on the development of therapeutical strategies targeting the mitochondria environment and their potential application for the treatment of AD itself. Full article
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