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The microvascular hypothesis, however, might be tempered by the concept that diabetes directly targets dorsal root ganglion sensory neurons. This neuron\u2010specific concept, supported by accumulating evidence, might account for important features of <jats:styled-content style=\"fixed-case\">DPN<\/jats:styled-content>, such as its early sensory neuron degeneration. Diabetic sensory neurons develop neuronal atrophy alongside a series of messenger ribonucleic acid (<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content>) changes related to declines in structural proteins, increases in heat shock protein, increases in the receptor for advanced glycation end\u2010products, declines in growth factor signaling and other changes. Insulin is recognized as a potent neurotrophic factor, and insulin ligation enhances neurite outgrowth through activation of the phosphoinositide 3\u2010kinase\u2013protein kinase B pathway within sensory neurons and attenuates phenotypic features of experimental <jats:styled-content style=\"fixed-case\">DPN<\/jats:styled-content>. Several interventions, including glucagon\u2010like peptide\u20101 agonism, and phosphatase and tensin homolog inhibition to activate growth signals in sensory neurons, or heat shock protein overexpression, prevent or reverse neuropathic abnormalities in experimental <jats:styled-content style=\"fixed-case\">DPN<\/jats:styled-content>. Diabetic sensory neurons show a unique pattern of micro<jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> alterations, a key element of messenger <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> silencing. For example, let\u20107i is widely expressed in sensory neurons, supports their growth and is depleted in experimental <jats:styled-content style=\"fixed-case\">DPN<\/jats:styled-content>; its replenishment improves features of <jats:styled-content style=\"fixed-case\">DPN<\/jats:styled-content> models. Finally, impairment of pre\u2010messenger <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> splicing in diabetic sensory neurons including abnormal nuclear <jats:styled-content style=\"fixed-case\">RNA<\/jats:styled-content> metabolism and structure with loss of survival motor neuron protein, a neuron survival molecule, and overexpression of <jats:styled-content style=\"fixed-case\">CWC<\/jats:styled-content>22, a splicing factor, offer further novel insights. The present review addresses these new aspects of <jats:styled-content style=\"fixed-case\">DPN<\/jats:styled-content> sensory neurodegeneration.<\/jats:p>","DOI":"10.1111\/jdi.12833","type":"journal-article","created":{"date-parts":[[2018,3,15]],"date-time":"2018-03-15T11:04:42Z","timestamp":1521111882000},"page":"1239-1254","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":147,"title":["Diabetic neuropathy and the sensory neuron: New aspects of pathogenesis and their treatment implications"],"prefix":"10.1111","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5131-1533","authenticated-orcid":false,"given":"Masaki","family":"Kobayashi","sequence":"first","affiliation":[{"name":"Department of Neurology and Neurological Science Graduate School of Medicine Tokyo Medical and Dental University Tokyo Japan"},{"name":"Department of Neurology Yokufukai Geriatric Hospital Tokyo 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