Premium
Iron‐Melanin Complex in Substantia Nigra of Parkinsonian Brains: An X‐Ray Microanalysis
Author(s) -
Jellinger K.,
Kienzl Elisabeth,
Rumpelmair G.,
Riederer P.,
Stachelberger H.,
BenShachar Dorit,
Youdim M. B. H.
Publication year - 1992
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1992.tb08362.x
Subject(s) - neuromelanin , substantia nigra , melanin , pars compacta , dopaminergic , neuropil , chemistry , dopamine , neurodegeneration , parkinson's disease , pathology , biophysics , neuroscience , biology , biochemistry , central nervous system , medicine , disease
Using energy‐dispersive x‐ray analysis on an electron microscope working in the scanning transmission electron microscopy mode equipped with a microanalysis system, we studied the subcellular distribution of trace elements in neuromelanin‐containing neurons of the substantia nigra zona compacta (SNZC) of three cases of idiopathic Parkinson's disease (PD) [one with Alzheimer's disease (AD)] and of three controls, in Lewy bodies of SNZC, and in synthetic dopamine‐melanin chemically charged or uncharged with Fe. Weak but significant Fe peaks similar to those of a synthetic melanin‐Fe 3+ complex were seen only in intraneuronal highly electron‐dense neuromelanin granules of SNZC cells of PD brains, with the highest levels in a case of PD plus AD. whereas a synthetic melanin‐Fe 2+ complex showed much lower iron peaks, indicating that neuromelanin has higher affinity for Fe 3+ than for Fe 2+ . No detectable Fe was seen in nonmelanized cytoplasm of SNZC neurons and in the adjacent neuropil in both PD and controls, in Lewy bodies in SNZC neurons in PD, and in synthetic dopamine‐melanin uncharged with iron. These findings, demonstrating for the first time a neuromelanin‐iron complex in dopaminergic SNZC neurons in PD, support the assumption that an iron‐melanin interaction contributes significantly to dopaminergic neurodegeneration in PD and PD plus AD.