Mitochondria, with Key Role in Neurodegeneration, May Offer Therapy Target, Review Suggests
Mitochondria play key roles in the processes that can lead to neurodegeneration and diseases like Alzheimer’s or Parkinson’s, a review of published studies into mitochondria-associated neurodegeneration found. The review also suggested that mitochondria are a therapeutic target worth investigating.
Details of these findings, “Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment,” were published in CNS Neurosciences & Therapeutics.
The progressive decline in the function and structure of neurons during neurodegeneration — defined as the progressive death of nerve cells and loss of brain tissue — involves complex processes and mechanisms that can make its causes difficult to identify. As a result, little is known about these processes or mechanisms.
Mitochondria are known, however, to be important to a number of cell functions, including energy production, respiration, metabolism, intracellular signaling, the production of free radicals, and programmed cell death (apoptosis). Several recent studies also suggest that impaired mitochondria could factor into the development of neurodegenerative processes.
Researchers surveyed published literature to gain a better understanding of how mitochondrial dysfunction might be involved in diseases like Alzheimer’s, Huntington’s, Parkinson’s, and amyotrophic lateral sclerosis, as well as whether mitochondria might be a therapeutic target for people with these diseases.
The survey noted that mitochondria are important to cell survival and cell death. When mitochondria are faced with stressors or changes in physiological conditions, they are capable of altering their morphology, number, and function to adapt to new conditions through a process based on mitochondrial fusion/fission machinery cycles.
Other findings suggested that changes in mitochondrial dynamics in combination with DNA/gene mutations contribute to mitochondrial dysfunction and the development of disease. Mitochondrial dysfunction could be manifested through imbalances in adaptation techniques like mitochondrial mixing (fusion) or fragmentation (fission), which in turn may lead to cell death and neurodegeneration.
Mitochondrial dysfunction is also often reflected in DNA damage, a decline in mitochondrial function, gene expression, and protein synthesis.
Patients with neurodegenerative diseases also have altered mitochondrial function in the brain, including the mitochondrial-based electrical conduction among neurons, the review reported.
“Regarding these data,” they concluded, mitochondria could be considered “a potential target for pharmacological-based therapies.”