DYSTROPHIC AXONAL SWELLINGS DEVELOP AS A FUNCTION OF AGE AND DIABETESIN HUMAN DORSAL-ROOT GANGLIA

Neuroaxonal dystrophy, characterized by swollen axon terminals and, to a lesser degree, enlarged initial segments of axons or perikaryal pro jections, develops in human dorsal root sensory ganglia as a function of aging and diabetes. Lesions are typically located within the satell ite cell capsule and are intimately applied to sensory neuronal perika rya, which are compressed and distorted but are otherwise normal. Swol len axons contain large numbers of neurofilaments that are immunoreact ive with antisera to highly phosphorylated neurofilament epitopes but fail to stain with antisera directed against hypophosphorylated neurof ilament epitopes. Other dystrophic swellings contain collections of tu bulovesicular profiles admired with neurotransmitter granules. Neuroax onal dystrophy involves subpopulations of intraganglionic axons and ap parent terminals, notably those containing CORP while apparently spari ng others, including noradrenergic sympathetic axons. Diabetic subject s develop lesions prematurely and in greater numbers than in aged subj ects. Individual dystrophic axons in diabetics and aged human subjects are identical in their light microscopic, immunohistochemical and ult rastructural appearance, suggesting the possibility of shared pathogen etic mechanisms.