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*Correspondence: Shaneel Chandra [email protected] Chapman [email protected] This article was submitted to Neuroinfectious Diseases, a section of the journal Frontiers in Neurology Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers

Several therapeutic strategies targeting either the primary or secondary defects of FRDA are under development following two main directions: (1) restoration of FXN levels using gene expression modulators, protein stabilizers and gene therapy and (2) alleviation of secondary cellular defects such as mitochondrial functions, iron accumulation, oxidative stress and ferroptosis (Zesiewicz et al., 2020

MMP-2 has been shown to have a role in synaptic plasticity (66) and be upregulated by noradrenaline (67)two biological mechanisms implicated in PTSD

High molecular weight adiponectin inhibits proliferation of hepatic stellate cells via activation of adenosine monophosphate-activated protein kinase

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