Age-dependent small fiber neuropathy: Mechanistic insights from animal models

Daniel G Taub; Clifford J Woolf

doi:10.1016/j.expneurol.2024.114811

Age-dependent small fiber neuropathy: Mechanistic insights from animal models

Exp Neurol. 2024 May 7:114811. doi: 10.1016/j.expneurol.2024.114811. Online ahead of print.

Authors

Daniel G Taub¹, Clifford J Woolf²

Affiliations

¹ F. M. Kirby Neurobiology Center and Department of Neurology, Boston Children's Hospital, Boston, MA, USA; Department of Neurobiology, Harvard Medical School, Boston, MA, USA. Electronic address: daniel.taub@childrens.harvard.edu.
² F. M. Kirby Neurobiology Center and Department of Neurology, Boston Children's Hospital, Boston, MA, USA; Department of Neurobiology, Harvard Medical School, Boston, MA, USA.

PMID: 38723859
DOI: 10.1016/j.expneurol.2024.114811

Abstract

Small fiber neuropathy (SFN) is a common and debilitating disease in which the terminals of small diameter sensory axons degenerate, producing sensory loss, and in many patients neuropathic pain. While a substantial number of cases are attributable to diabetes, almost 50% are idiopathic. An underappreciated aspect of the disease is its late onset in most patients. Animal models of human genetic mutations that produce SFN also display age-dependent phenotypes suggesting that aging is an important contributor to the risk of development of the disease. In this review we define how particular sensory neurons are affected in SFN and discuss how aging may drive the disease. We also evaluate how animal models of SFN can define disease mechanisms that will provide insight into early risk detection and suggest novel therapeutic interventions.

Keywords: Aging; C-LTMRs; C-tactile afferents; Lipids; Mitochondria; Nav1.7; Peripheral neuropathy; Scn9a; Small fiber neuropathy; Sodium channels.

Publication types

Review