Dystrophic Axonal Swellings Develop as a Function of Age and Diabetes in Human Dorsal Root Ganglia

Neuroaxonal dystrophy, characterized by swollen axon terminals and, to a lesser degree, enlarged initial segments of axons or perikaryal projections, develops in human dorsal root sensory ganglia as a function of aging and diabetes. Lesions are typically located within the satellite cell capsule and...

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Bibliographic Details
Published in:Journal of neuropathology and experimental neurology 1997-09, Vol.56 (9), p.1028-1043
Main Authors: SCHMIDT, ROBERT E, DORSEY, DENISE, PARVIN, CURTIS A, BEAUDET, LUCIE N, PLURAD, SANTIAGO B, ROTH, KEVIN A
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Aging - physiology
Antigenic determinants
Axons - ultrastructure
Biological and medical sciences
Child
Continental Population Groups
Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction
Diabetes Mellitus - ethnology
Diabetes Mellitus - pathology
Diabetes Mellitus - physiopathology
Female
Ganglia, Spinal - pathology
Humans
Male
Medical sciences
Middle Aged
Nervous system (semeiology, syndromes)
Neurology
Sex Characteristics
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Summary:Neuroaxonal dystrophy, characterized by swollen axon terminals and, to a lesser degree, enlarged initial segments of axons or perikaryal projections, develops in human dorsal root sensory ganglia as a function of aging and diabetes. Lesions are typically located within the satellite cell capsule and are intimately applied to sensory neuronal perikarya, which are compressed and distorted but are otherwise normal. Swollen axons contain large numbers of neurofilaments that are immunoreactive with antisera to highly phosphorylated neurofilament epitopes but fail to stain with antisera directed against hypophosphorylated neurofilament epitopes. Other dystrophic swellings contain collections of tubulovesicular profiles admixed with neurotrasnsmitter granules. Neuroaxonal dystrophy involves subpopulations of intraganglionic axons and apparent terminals, notably those containing CGRP, while apparently sparing others, including noradrenergic sympathetic axons. Diabetic subjects develop lesions prematurely and in greater numbers than in aged subjects. Individual dystrophic axons in diabetics and aged human subjects are identical in their light microscopic, immunohistochemical and ultrastructural appearance, suggesting the possibility of shared pathogenetic mechanisms.
ISSN:0022-3069
1554-6578
DOI:10.1097/00005072-199709000-00008