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Neuronal pigmented autophagic vacuoles: lipofuscin, neuromelanin, and ceroid as macroautophagic responses during aging and disease
Author(s) -
Sulzer David,
Mosharov Eugene,
Talloczy Zsolt,
Zucca Fabio A.,
Simon John D.,
Zecca Luigi
Publication year - 2008
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.1471-4159.2008.05385.x
Subject(s) - lipofuscin , vacuole , neuromelanin , autophagy , microbiology and biotechnology , organelle , biology , lysosome , mitochondrion , endocytic cycle , ultrastructure , chemistry , biochemistry , cytoplasm , substantia nigra , cell , neuroscience , anatomy , endocytosis , dopamine , apoptosis , enzyme , dopaminergic
The most striking morphologic change in neurons during normal aging is the accumulation of autophagic vacuoles filled with lipofuscin or neuromelanin pigments. These organelles are similar to those containing the ceroid pigments associated with neurologic disorders, particularly in diseases caused by lysosomal dysfunction. The pigments arise from incompletely degraded proteins and lipids principally derived from the breakdown of mitochondria or products of oxidized catecholamines. Pigmented autophagic vacuoles may eventually occupy a major portion of the neuronal cell body volume because of resistance of the pigments to lysosomal degradation and/or inadequate fusion of the vacuoles with lysosomes. Although the formation of autophagic vacuoles via macroautophagy protects the neuron from cellular stress, accumulation of pigmented autophagic vacuoles may eventually interfere with normal degradative pathways and endocytic/secretory tasks such as appropriate response to growth factors.