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Mitotoxicity in distal symmetrical sensory peripheral neuropathies
Gary J Bennett1, Timothy Doyle2, Daniela Salvemini2
1Department of Anaesthesia, Faculty of Dentistry, and The Alan Edwards Centre for Research on Pain, McGill University, 3655 Promenade Sir William Osler, Montréal, QC H3G 1Y6, Canada.
Nature Reviews. Neurology
|May 21, 2014
Summary
Mitochondrial dysfunction in sensory neurons may cause similar symptoms across various neuropathies, including those from chemotherapy, HIV, and diabetes. Improving mitochondrial function could be a potential treatment strategy.
Area of Science:
- Neuroscience
- Cell Biology
- Pharmacology
Background:
- Chronic distal symmetrical sensory peripheral neuropathy is a frequent complication of cancer chemotherapy, HIV treatment, and diabetes.
- Despite differing causes, these neuropathies share similar clinical signs and symptoms.
Purpose of the Study:
- To investigate the common underlying cause of similar neuropathic symptoms across various etiologies.
- To explore the role of mitochondrial dysfunction in primary afferent sensory neurons.
Main Methods:
- Review of data from animal models of neuropathic pain.
- Analysis of the mechanisms of mitochondrial dysfunction induced by chemotherapeutic drugs, HIV proteins, nucleoside reverse transcriptase inhibitors, and excess glucose.
- Examination of neuronal energy deficits and degeneration patterns, particularly in intraepidermal nerve fibres.
Main Results:
- Mitochondrial dysfunction in primary afferent sensory neurons is suggested as a common cause for similar neuropathic symptoms.
- Mitotoxic agents (chemotherapy, HIV drugs) and excess glucose induce mitochondrial dysfunction.
- Mitochondrial injury leads to neuronal energy deficits, spontaneous nerve impulses, and degeneration of terminal nerve fibers.
Conclusions:
- Mitochondrial dysfunction is a unifying mechanism underlying diverse peripheral neuropathies.
- Targeting mitochondrial injury or function represents a promising therapeutic avenue for treating these conditions.
