Identification of components of immunoglobulins in senile plaques by means of fluorescent antibody technique

Ishii, Tsuyoshi; Haga, S.; Shimizu, Fujio

doi:10.1007/bf00689569

Cited by 105 publications

(34 citation statements)

References 10 publications

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“…Dlnue: Involvement of autoimmunity in the patholenesis of AD has been suspected for man y yean. Presence of I!JG in senile plaques has already been reported by severalaroups (Ishii et al 1975, Ishii and Haaa 1976, Ihara et al 1981). …”

Section: Extracellular Amyloid Ln Alzheimer's Diseasesupporting

confidence: 54%

Amyloid enhancing factor activity is associated with ubiquitin

Alizadeh-Khiavi

Normand

Chronopoulos

et al. 1992

Vichows Archiv A Pathol Anat

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Section: Extracellular Amyloid Ln Alzheimer's Diseasesupporting

confidence: 54%

Amyloid enhancing factor activity is associated with ubiquitin

Alizadeh-Khiavi

Normand

Chronopoulos

et al. 1992

Vichows Archiv A Pathol Anat

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“…Immunological changes have been associated with the pathogenesis and clinical progression of Alzheimer's disease [1][2][3][4][5][6][7]. In this direction, our preliminary data have demonstrated an increased reactivity of natural killer (NK) cells to cytokines (i.e.…”

Section: Introductionmentioning

confidence: 62%

Decreased Immunosuppressive Effect of Cortisol on Natural Killer Cytotoxic Activity in Senile Dementia of the Alzheimer Type

Solerte

Cerutti

Severgnini

et al. 1998

Dement Geriatr Cogn Disord

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Former studies have indicated alterations of the cytotoxic activity of natural killer (NK) cells in senile dementia of the Alzheimer type (SDAT). These changes may be related to the increased reactivity of NK cells with cytokines, even if an impairment of the immunosuppressive effect of glucocorticoids cannot be excluded. In the present study we have demonstrated a lower immunosuppressive effect of cortisol on NK cytolytic function in patients with SDAT than in healthy elders and in patients with dementia of multi-infarct origin (MID). This suppression is completely lacking when cortisol is employed at low concentrations (10^–7 M) and is significantly reduced after incubation at physiological (10^–6 M; p < 0.001) and supraphysiological concentrations (10^–5 M; p < 0.001). The addition of IL-2 (50 and 100 IU/ml/cells) significantly antagonizes the effects of cortisol in SDAT, whereas the cortisol-dependent immunosuppression is partially maintained in healthy elders and in patients with MID. Our data indicate that the defect of the immunosuppressive effect of cortisol may play a role in NK dysregulation in SDAT, contributing to the cytokine-mediated NK overactivity in this disease.

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“…10 The exact nature of the mechanism leading to amyloid deposition within cerebral blood vessels is still unknown. 25 Several studies have demonstrated yglobulins 26 " 29 or prealbumin 30 in senile plaques and amyloid angiopathic lesions. Such deposition, however, might also be due to nonspecific exudation of serum protein through disrupted endothelial layers.…”

Section: Discussionmentioning

confidence: 99%

Autopsy study of incidence and distribution of cerebral amyloid angiopathy in Hisayama, Japan.

Masuda

Tanaka

Ueda

et al. 1988

Stroke

150

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The incidence of cerebral amyloid angiopathy in a general population was evaluated in brains of 400 consecutive autopsies of residents of Hisayama, Japan (November 1971-October 1983). Six samples taken from frontal lobe, parietal lobe, temporal lobe, occipital lobe, hippocampus, and basal ganglia of the same side of each brain were stained with both hematoxylin and eosin and Congo red. The specimens were surveyed microscopically with polarized light for deposition of amyloid in the vascular wall. In 26 cases with brain hemorrhage, the region surrounding the hemorrhagic sites was further examined to study the probable causal relation between cerebral amyloid angiopathy and brain hemorrhage. Cerebral amyloid angiopathy was found in 40 of 218 men (18.3%) and 51 of 182 women (28.0%). The incidence increased with age in both sexes. The frontal lobe was most frequently affected (66 cases), followed by parietal lobe (65), occipital lobe (49), temporal lobe (44), and hippocampus (32); the putamen was never affected. The incidence of cerebral amyloid angiopathy did not correlate with blood pressure or with the severity of cerebral atherosclerosis. Among the 26 cases in which there was brain hemorrhage, only one cerebellar hemorrhage, in an 85-year-old man, was attributed to cerebral amyloid angiopathy. This case showed four microaneurysms in vessels, with cerebral amyloid angiopathy surrounding the hemorrhagic site. Thirty similar lesions were observed in eight cases without brain hemorrhage. Cerebral amyloid angiopathy may play an etiologic role in the development of brain hemorrhage through formation of angionecrosis and microaneurysm.

show abstract

Identification of components of immunoglobulins in senile plaques by means of fluorescent antibody technique

Cited by 105 publications

References 10 publications

Amyloid enhancing factor activity is associated with ubiquitin

Amyloid enhancing factor activity is associated with ubiquitin

Decreased Immunosuppressive Effect of Cortisol on Natural Killer Cytotoxic Activity in Senile Dementia of the Alzheimer Type

Autopsy study of incidence and distribution of cerebral amyloid angiopathy in Hisayama, Japan.

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