ISSN:
1432-0533
Keywords:
Key words Huntington's disease
;
Human brain
;
Thalamus
;
Nuclei centromedianus-parafascicularis
;
Neurone number
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract The centromedian-parafascicular complex represents a nodal point in the neuronal loop comprising striatum – globulus pallidus – thalamus – striatum. Striatal neurone degeneration is a hallmark in Huntington's disease and we were interested in estimating total neurone and glial number in this thalamic nuclear complex. Serial 500-μm-thick gallocyanin-stained frontal sections of the left hemisphere from six cases of Huntington's disease patients (three females, three males) and six age- and sex-matched controls were investigated applying Cavalieri's principle and the optical disector. Mean neurone number in the controls was 646,952 ± 129,668 cells versus 291,763 ± 60,122 in Huntington's disease patients (Mann-Whitney U-test, P 〈 0.001). Total glial cell number (astrocytes, oligodendrocytes, microglia, and unclassifiable glial profiles) was higher in controls with 9,544,191 ± 3,028,944 versus 6,961,989 ± 2,241,543 in Huntington's disease patients (Mann-Whitney U-test, P 〈 0.021). Considerable increase of fibrous astroglia within the centromedian-parafascicular complex could be observed after Gallyas' impregnation. Most probably this cell type enhanced the numerical ratio between glial number and neurone number (glial index: Huntington's disease patients = 24.4 ± 8.1; controls = 15.0 ± 5.2; Mann-Whitney U-test, P 〈 0.013). The neurone number in the centromedian-parafascicular complex correlated negatively, although statistically not significantly, with the striatal neurone number. This lack of correlation between an 80% neuronal loss in the striatum and a 55% neurone loss in the centromedian-parafascicular complex points to viable neuronal circuits connecting the centromedian-parafascicular complex with cortical and subcortical regions that are less affected in Huntington's disease.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004010050408
