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S A Chance

Publications and source records attributed to S A Chance.

7 recordsLinked to original sources

Minicolumnar structure in Heschl's gyrus and planum temporale: Asymmetries in relation to sex and callosal fiber number.

AIM: To investigate the cytoarchitectural basis of asymmetries in human auditory cortex. Minicolumn spacing and number, and regional cortical volume and surface area were measured in the primary auditory region (Heschl's gyrus, HG) and posterior auditory association region (planum temporale, PT) in 17 neurologically normal adults (10 female, seven male). PT surface area, minicolumn spacing and minicolumn number were greater in the left hemisphere. HG surface area was larger in the left hemisphere. Asymmetries of minicolumn number in primary and association auditory regions correlated with axonal fiber numbers in the subregions of the corpus callosum through which they project. PT minicolumn number was more asymmetrical in men than women but total number was similar in the two sexes. We conclude that asymmetry of the surface area of the PT is a function of minicolumn spacing. Fewer callosal projections between the plana are found when the minicolumn spacing is more asymmetrical.

Aged↗

Neocortical neuronal, synaptic, and glial loss in multiple sclerosis.

BACKGROUND: Recent pathologic investigations have shown that neocortical lesions are frequent in multiple sclerosis (MS). Structural MRI has shown that neocortical atrophy occurs early and can be substantial, but the specific substrate for this atrophy has not been defined quantitatively. OBJECTIVE: To investigate cortical thickness as well as neuronal, glial, and synaptic densities in MS. METHODS: We studied brain samples from 22 patients with MS and 17 control subjects. Neocortical lesions and cortical thickness were assessed on sections stained for myelin basic protein. Neuronal, glial, and synaptic densities were measured in type I leukocortical lesions, nonlesional neocortex, and non-MS control cortex. Immunoautoradiography was used to quantify synaptic densities. RESULTS: Neocortical lesions were common in patients with MS. Subpial type III (44%) and leukocortical type I (38%) lesions were more abundant than intracortical type II (18%) lesions. An overall relative neocortical thinning of 10% (p = 0.016) was estimated for the patients. Within the type I lesions, we found evidence for substantial cell (glial, 36%, p = 0.001; neuronal, 10%, p = 0.032) and synaptic (47% decrease in synaptophysin, p = 0.001) loss. Nonlesional neocortex did not show significant relative changes in neuronal, glial, or synaptic density. CONCLUSIONS: Neocortical neuronal and glial degeneration is significant in multiple sclerosis. Synaptic loss was particularly striking in the neocortical lesions, which should make a major independent contribution to the expression of pathology. New therapies should be directed toward limiting this damage.

Adult↗

Subtle changes in the ageing human brain.

Subtle changes in the human brain constitute a third element in addition to plaques and tangles as markers of vulnerability to Alzheimer's disease (AD). Neurofibrillary tangle (NFT) distribution shows the closest relationship to the severity of dementia. Two features of the distribution (regional selectivity and columnar clustering) provide clues about the structural changes due to normal ageing that may precede tangle formation. It is hypothesized that the columnar organization of the cortex, determines the pattern of pathological spread in AD and, consequently, the pattern of function loss. Minicolum thinning occurs in normal ageing and echoes the selective regional distribution of NFT formation in AD. NFT vulnerability appears to emerge from hierarchical variation in neural plasticity associated with the hierarchical variation in size and spacing of mini and macro-columns in the cortex. Regional differences may involve regional variation in gene expression. Dietary Omega 3 fatty acid intake has been shown to have neuroprotective effects on the cytoarchitectural features that contribute to this cortical hierarchy.

Aging↗

Vulnerability to Alzheimer's pathology in neocortex: the roles of plasticity and columnar organization.

Two principal findings in the Pearson et al. paper are commented on here. The first is the regional selectivity within the cerebrum of neurofibrillary tangle (NFT) formation in Alzheimer's disease (AD) which targets association cortex and the primary olfactory cortex alone among regions of primary sensory cortex. The second finding is the clustering of NFT in columns of supra- and infra-granular layers of association cortex. We review recent evidence confirming these findings and comment on their possible significance. We consider that the most attractive hypothesis to explain the vulnerability of the olfactory system and association cortex is the persistent neural plasticity of these regions. On this basis there would be no need to postulate a progressive spreading process. The columnar distribution of clustered NFT can be well understood in the context of recent concepts of columnar organization of the cerebral cortex. The original interpretation that this distribution of NFT reflects pathology in neurons subserving cortico-cortical and cortico-subcortical connections seems to us to have stood the test of time.

Alzheimer Disease↗

Reduced density of calbindin-immunoreactive interneurons in the planum temporale in schizophrenia.

Reduced density of calbindin-containing interneurons in the prefrontal cortex in schizophrenia has been reported (Beasley et al 2002; Biol Psych 52:708-715). Calbindin is a calcium-binding protein (CBP) present in a subpopulation of GABAergic neurons restricted mainly to layer II of the cortex. A paraffin-embedded, 10-mum-thick section from the planum temporale (PT) of each hemisphere was prepared from 12 patients with schizophrenia and 12 controls. Calbindin-containing cells were stained using an antibody (D-28K). Counting frames were superimposed to sample within layer II of the PT. A bilateral reduction (20%) in calbindin cell density was found in patients (controlling for fixation time). Furthermore, mean calbindin cell cross-sectional area was increased in female patients and reduced in male patients. Reduced CBP expression (reducing the excitability of interneurons) or reduced number of CBP-containing cells may cause disinhibition of pyramidal cells. The majority of calbindin-containing cells in the mature brain are double-bouquet cells with vertically oriented dendrites and axon bundles. By exercising inhibitory modulation of pyramidal cells in a columnar arrangement, they make possible cohesive vertical inhibition of minicolumns. Loss of columnar inhibition may result in reduced minicolumnar segregation and altered cell size may reflect altered minicolumn size.

Adult↗

The cytoarchitecture of sulcal folding in Heschl's sulcus and the temporal cortex in the normal brain and schizophrenia: lamina thickness and cell density.

Developmental and psychiatric disorders, including schizophrenia, may be associated with altered cortical thickness and folding. Two studies were performed: (1) to assess cortical layering around a sulcus; cortical thickness, relative thickness of the supragranular (I-III):infragranular (IV-VI) layers, and cell density were assessed at anatomically defined points around Heschl's sulcus in tissue from 10 controls and 10 schizophrenia patients. (2) To sample sulci of contrasting prominence; sulcal depth, width, lamina thickness, and cell density from laminae II-VI were taken from various sulci within the temporal lobes from another group of 6 controls and 10 patients. Reduced cell density was found in the fundi of sulci in schizophrenia. Independent of diagnosis; increased sulcal prominence in temporal cortex accompanies reduced lamina thickness (particularly layers V and VI), deep layers show negative relationships between cell density and layer thickness, and total cortex width in Heschl's sulcus reduces by half at the bottom compared to the top. Furthermore, compared to the supragranular layers, the infragranular division is relatively thicker at the top of a gyrus, equal in the wall of the sulcus and relatively thinner at the bottom. Many effects of sulcal folding on laminar proportions in controls are similar in schizophrenia. However, cell density is less at the bottom of some sulci in the temporal lobe in schizophrenia. Sampling methods should consider that cortical folding affects cell and lamina distribution in the sampled region in a highly localised manner.

Aged↗

Fiber content of the fornix in schizophrenia: lack of evidence for a primary limbic encephalopathy.

OBJECTIVE: There have been claims that schizophrenia is a disease of the limbic circuit and that the volume of the hippocampus and its content of neurons are low in schizophrenia. The fornix is a major pathway through which neurons project to and from the hippocampus. The authors investigated whether the fiber number or structure of the fornix is abnormal in schizophrenia, as was suggested by an earlier MRI study. METHOD: A section of fornix was removed from each hemisphere of postmortem brains of 16 male and 13 female schizophrenic patients and a comparison group of 19 men and 14 women. Cross-sectional area, fiber density, and total fiber number were examined for differences between diagnostic groups and between genders. RESULTS: The men had a lower fiber density in the fornix than the women. Fiber density on the left side was greater in the schizophrenic men than in the comparison men. For total fiber number (density multiplied by area) there were no differences between groups. Density was found to decrease with increasing area, suggesting that these measures may be affected by degree of myelination. CONCLUSIONS: The fornix does not show the abnormalities in cross-sectional area or total fiber number that would be expected if the primary impact of schizophrenia is on the hippocampus and limbic system. The greater density on the left in schizophrenic men suggests an effect of schizophrenia on myelination related to sex and asymmetry, which may reflect one aspect of a global delay in brain development.

Adult↗