The acoustic cortex in frontotemporal dementia: a Golgi and electron microscope study.
Title | The acoustic cortex in frontotemporal dementia: a Golgi and electron microscope study. |
Publication Type | Journal Article |
Year of Publication | 2011 |
Authors | Baloyannis, S. J., Mauroudis I., Manolides S. L., & Manolides L. S. |
Journal | Acta Otolaryngol |
Volume | 131 |
Issue | 4 |
Pagination | 359-61 |
Date Published | 2011 Apr |
ISSN | 1651-2251 |
Keywords | Auditory Cortex, Dendrites, Female, Frontotemporal Dementia, Golgi Apparatus, Humans, Male, Microscopy, Electron, Synapses |
Abstract | CONCLUSION: The neuronal loss and the alteration of the synapses in the acoustic cortex in frontotemporal dementia (FTD) may be related to the impairment of communication and symbolic sound perception, which is noticed in the majority of the cases.OBJECTIVES: FTD is a heterogeneous neurodegenerative disorder, causing progressive decline of intellectual faculties, impairment of behavior and social performance, and impairment of speech eloquence, associated with various neurological manifestations based on a variable neuropathological background. We attempted to determine the morphological alterations of the dendrites and the dendritic spines in the acoustic cortex of 10 cases who fulfilled the diagnostic criteria for FTD.METHODS: For the histological study we applied (a) routine neuropathological techniques and (b) rapid Golgi method. We proceeded to electron microscopy for the ultrastructural study of the synapses and the morphological and morphometric study of the organelles, the dendrites, and the dendritic spines.RESULTS: The morphological and morphometric analysis revealed substantial neuronal loss and synaptic alterations in the acoustic cortex in all the cases of FTD and particularly in Pick disease and in primary progressive aphasia. Mitochondria alterations and changes of the Golgi apparatus were seen mostly in Pick disease. |
DOI | 10.3109/00016489.2010.539267 |
Alternate Journal | Acta Otolaryngol. |
PubMed ID | 21189051 |