| Objective:To study the histopathologial changes in amygdala of Alzheimer's disease,Pakinson disease,progressive supranuclear palsy and frontotemporal lobe degeneration,which mainly include?-amyloid protein,tau protein,a-synuclein protein,TDP-43 protein and argyrophilic grains.Materials and methods:The amygdaloid nucleus specimens from 16 autopsy brain tissues with complete clinical data and clear pathological diagnosis were studied,which include 5 cases of Alzheimer's disease(2 cases pathologically diagnosed as Alzheimer's disease with argyrophilic grain disease),3 cases of Pakinson disease,2 cases of progressive supranuclear palsy,1 case of frontotemporal lobe degeneration and 5 cases of normal control.Hematoxylin-eosin,Luxol Fast Blue,Gallyas-Braak silver staining and immunohistochemical staining were used.The neuron loss,gliosis,A?pathology,tau pathology,a-synuclein pathology,TDP-43pathology,and argyrophilic grains in the amygdala were observed.Results:1.Both common neurodegenerative diseases and normal controls had different degrees of neuron loss and glial cell proliferation in the amygdala,but neurodegenerative diseases were more extensive and more severe2.Senile plaques and neurofibrillary tangles were observed in all the five Alzheimer's disease amygdalas,among which three cases had a positive structure of a-synuclein,two out of the three cases also had a positive structure of TDP-43,and argyrophilic grains structure could also be observed in these two cases.The frequency of AP pathology and tau pathology was the highest in the amygdalas of AD,and the A? pathological load and tau pathological load were also the highest in the amygdalas of AD and its subregions.A? pathology was most severe in the ventral of the basolateral nuclear group of the AD amygdala,followed by the cortico-medial group and the dorsal of basolateral nuclear group is the lithtest.AD amygdaloid tau pathological load basolateral nuclear group is larger than medial cortical nuclear group.The tau pathological load in basolateral nuclear group is larger than cortico-medial group.3.In the three cases of Pakinson disease,the amygdaloid senile plaques were negative,two cases showed slight tau pathological changes,and only one case showed slight TDP-43 positive structure.Pathological changes of the a-synuclein protein were observed in the amygdalas of PD in all three cases,with mild to severe variations.The histopathological frequency of a-synuclein in the amygdala of PD was the highest,and the histopathological load of a-synuclein in the amygdala and its subregions of PD was also the highest.The pathology of a-synuclein is the most severe in the central nucleus of PD,followed by the ventral of basolateral nucleus group,and the most mild in the cortico-medial nucleus group and the dorsal of basolateral nucleus group.4.In two cases of progressive supranuclear palsy,tau protein in the amygdala of PSP was positive,and tufted astrocytes and various degrees of neurofibrillary tangles were observed in all cases,but no senile plaques,a-synuclein protein pathology and TDP-43 protein pathology were observed.Tau frequency in the amygdala of PSP was similar to that of AD,while tau load in the amygdala and its subregions of PSP was only lower than that of AD.Tau pathology was most severe in the ventral of the cortico-medial group and the basal lateral nucleus group of PSP,and the dorsal of the basal lateral nucleus group was the lightest.5.In this case of frontotemporal lobe degeneration,the amygdalas only showed mild a-synuclein pathology,while the other proteins were all negative.6.All amygdalas of the five normal controls were tau positive,but most of them were mild to moderate in severity.Among the 5 normal controls,mild senile plaques were observed in 2 cases of amygdalas,and scattered TDP-43 pathology was observed in 2 cases.Meanwhile,1 patient had a sporadic a-synuclein pathology.The frequency of amygdalas A? pathology in normal control was lower than that in AD,and the pathological load in each subregion was lower than that in AD.Tau pathological frequency in normal control amygdala was the same as AD,but tau pathological load was lower than AD.7.Among the 16 cases of amygdalas,4 cases presented argyrophilic grains pathology with a detection rate of 25%,including 2 cases of AD,1 case of PSP and 1 case of normal control.8.The pathological frequency of TDP-43 in AD and normal controls was slightly higher than that of PD,and the pathological load of TDP-43 in AD and normal controls was almost the same,with a small scattered distribution TDP-43 positive morphologies included neuron inclusion bodies and dystrophic filaments.Conclusion:1.Both common neurodegenerative disease and normal control amygdalas have different degrees of neuron loss and glial cell proliferation.2.The frequency of the characteristic protein pathology of AD and PD in the amygdala was higher than that of other groups.In addition,the load of A? pathology and tau pathology in the amygdala and its subregions of AD and the load of-synuclein pathology in the amygdala and its subregions of PD were higher than that of other groups,respectively.The distribution of A pathology and tau pathology in AD and a-synuclein pathology in the amygdaloid nuclei of PD is different to some extent.3.The amygdalas of PSP have degeneration of neurons and glial cells4.The occurrence of argyrophilic grains in the aged brain is not low,and it often coexists with other neurodegenerative diseases,which have different detection rates in different neurodegenerative diseases.5.The amygdalas of normal control and neurodegenerative diseases can contain several or all pathological structures of A? pathology,tau pathology,a-synuclein pathology,TDP-43 pathology and argyrophilic grains at the same time.The co-existence of multiple pathological structures in the amygdala may complicate the clinical manifestations and make diagnosis of neurodegenerative diseases difficult. |
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