Poster
# 118
Poster |
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6th Internet World Congress for Biomedical Sciences |
Domizio Suvā(1), Isabelle Favre(2), Rudolf Kraftsik(3), Monica Esteban(4), Alexander Lobrinus(5), Judit Miklossy(6)
(1)(2)(4)(5)(6)CHUV, Institute of Pathology - Lausanne. Switzerland
(3)IBCM - Lausanne. Switzerland
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[Neuroscience] |
[Pathology] |
The results of the quantitative analysis of plaques and tangles obtained by both examiners were similar without statistically significant difference, indicating their reproducibility and reliability. We thus used both datasets, giving us a mean value for ten cortical fields for both plaques and tangles. These data are presented in Table1.
In the brain of all 17 AD cases the primary motor cortex was severely affected by senile plaques (fig. 1, A). The percentage of cortical surface occupied by plaques in the primary motor cortex was similar to that found in other cortical areas (Table1, fig. 1 and fig. 2A). In 2 cases the percentage of cortical surface occupied by senile plaques was even higher in the primary motor cortex than in the associative cortical areas (Table1, cases 4, 5), and in two other cases it was higher than in the parietal associative cortex (Table1, cases 6, 16).
The number of neurofibrillary tangles in the primary motor cortex was lower than in the entorhinal cortex, and slightly lower than in the associative cortical areas (Table1, fig. 2B) with the exception of two cases. Case 9 showed higher number of tangles in the primary motor cortex than in the associative cortical areas and in two other cases (cases 12 and 13) the number of tangles was higher than in the entorhinal cortex (Table1).
The majority of cases with discrete to moderate AD-type cortical changes showed the presence of senile plaques in all examined areas including the primary motor cortex, except in one case, in which no plaques were found (case 21) in the primary motor and sensory cortex. Neurofibrillary tangles in these 7 cases were restricted to the entorhinal cortex, except in the two cases where few tangles were counted in the associative cortical areas. In one case (case 24 of Table1) some neurofibrillary tangles were also found in the primary motor cortex. There were no plaques or tangles in any cortical areas of the brain in the control group.
There were some regional differences in the distribution of plaques and tangles with respect to different cortical areas. In 1 case (Table1, case 3) the cortical surface occupied by plaques was more than five times higher in the frontal than in parietal cortex, respectively.
The distribution of the cases with respect to the increasing percentage of cortical surface (by 2% intervals) occupied by plaques and the increasing number of neurofibrillary tangles (by intervals of 3 tangles) in the primary motor cortex is illustrated on fig. 3 A and B, respectively. In the majority of AD cases (11 of the 17) the percentage of cortical surface occupied by senile plaques in the primary motor cortex was high (14-20%). In the 7 cases with discrete to moderate cortical changes it was equal or lower than 12%.
In the majority of AD cases the number of tangles in the motor cortex varied between 3 and 18. In all the seven cases with discrete to moderate cortical changes the number of tangles was less than 3 and in the 5 control cases it was zero.
The primary sensory cortex was also severely involved by AD-type changes by both plaques and tangles, in proportions similar to that of the primary motor cortex (Table1).
In the group of the 17 AD cases the statistical analysis did not reveal significant difference between cortical areas regarding the percentage of cortical surface occupied by senile plaques in the primary motor cortex and in the other cortical areas. The number of tangles was significantly higher in the entorhinal cortex when compared to the other cortical areas (p<0.001). Their number was somewhat lower in the primary motor and primary sensory cortex than in the associative cortical areas, with a difference of borderline significance (p=0.04) There was no significant difference between the number of tangles in frontal and parietal associative cortical areas, or between the primary motor and sensory cortex.
The severity of the primary motor cortex involvement by senile plaques strongly correlated with that of primary sensory (R=0.8; p<0.001), enthorhinal (R= 0.7; p=0.004) and frontal associative cortex (R= 0.6; p=0.01) (fig. 4). Concerning the severity of the cortical involvement by neurofibrillary tangles a high correlation was found between the primary motor cortex and the sensory (R=0.9; p<0.001), parietal (R=0.7; p=0.009) and frontal associative cortex (R=0.6; p=0.007).
Due to the severe degenerative process, the cyto- and myeloarchitectonic hallmarks to delineate cortical layers are less distinct in the 17 AD cases than in the control cases. We did not observed laminar distribution of senile plaques in the primary motor cortex (fig. 5). In a few cases a slight tendency for a laminar distribution with a higher density of plaques in layers III and V was noticed. A tendency for laminar distribution of neurofibrillary tangles was observed in the primary motor cortex, where tangles were more numerous in the superior part of layer III and in layer V (fig. 5). In the primary sensory cortex, a laminar distribution, with high density of plaques in the inferior part of layer III and in layer IV was observed. We did not observe laminar distribution of neurofibrillary tangles in the primary sensory cortex. In the 17 AD cases on haematoxylin-eosin and cresyl-violet-stained sections neuronal loss was observed in all cortical layers of the primary motor cortex including layers Va and Vb. The loss of neurons in layer V, including those of the Betz cells in layer V/b in a familial AD case is illustrated in fig. 1E and F. The severity of neuronal loss, including those of Betz cells varied in different cases. We did not observe neuronal loss in the 5 control cases.
In the 9 severe AD cases (group AD, cases 1, 7, 8, 9, 10, 11, 12, 14, 16) where the primary visual cortex was available for analysis, a high number of senile plaques and a high to moderate number of neurofibrillary tangles was observed in this area. Only in one case (case 10) we did not find tangles in the primary visual cortex.
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[Neuroscience] |
[Pathology] |
