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T Kitamoto

Publications and source records attributed to T Kitamoto.

At least 163 records · Page 9Linked to original sources
PubMed1988

Gerstmann-Sträussler-Scheinker disease: immunohistological and experimental studies.

The older brother of the patient from whom the Fukuoka-1 strain was isolated was found to have numerous kuru plaques, the main finding common to both siblings. Other clinicopathological features including spongiform change were absent in the older brother. Immunostaining using anti-kuru plaque core protein and anti-beta-protein peptide revealed many kuru plaques and a few senile plaques in the older brother. Experimental transmission of the disease to laboratory animals was successful, using tissues from both siblings, through inoculation of fresh brain homogenates, purified prion protein, and formalin-fixed brain homogenates. Prion protein fractions from the patient's brain shortened the incubation periods and formalin-fixed mouse brains did not lengthen the periods. The disease in the two brothers can be classified as Gerstmann-Sträussler-Scheinker disease, a familial variant of Creutzfeldt-Jakob disease. Gerstmann-Sträussler-Scheinker disease manifests a variety of clinicopathological features. Immunohistological verification of kuru plaques has major diagnostic value in assessing dementia.

Aged↗
PubMed1988

Immunohistochemical verification of senile and kuru plaques in Creutzfeldt-Jakob disease and the allied disease.

We investigated paraffin-embedded brain sections from 41 patients with Creutzfeldt-Jakob disease (CJD) and from 9 with Gerstmann-Sträussler syndrome (GSS) using anti-human prion protein (PrP) antisera (anti-GSS kuru plaque cores and anti-PrP synthetic peptide) and anti-beta protein antiserum. The anti-human PrP antiserum reacted with the plaques in CJD and GSS, with or without degenerative neurites (neuritic components). In addition, the anti-beta protein antiserum immunolabeled kuru plaque-like compact plaques in some cases of CJD. Therefore, previous morphological classifications of the plaques may not always be valid. Senile plaques labeled with anti-beta protein antiserum were evident in 65% of the CJD brains and 50% of GSS brains from patients in their 60s, and in 73% of brains from CJD patients in their 70s, but not in brains from patients under 60 years of age. The incidence of the senile plaques was compatible with the normal aging process and was apparently not accelerated by the disease process of CJD or GSS. These immunostaining approaches using anti-human PrP and anti-beta protein antisera allow classification of plaque types and increase the reliability of the pathological diagnosis in persons with dementia.

Adult↗
PubMed1988

Focal intracerebral accumulation of a novel type of amyloid protein. An early stage of cerebral amyloidoma?

The brain of a 60-year-old patient with bronchial carcinoma presented a focal amyloid deposit in the white matter associated with myelin and axonal destruction. An additional lesion was found in the basal ganglia. This silent focal intracerebral accumulation of amyloid substance may be a prestadium of a "cerebral amyloidoma". The histochemical and immunohistochemical analysis of the accumulated amyloid indicated that it may belong to a novel type of amyloid.

Amyloid↗
PubMed1988

Renal amyloidosis. Correlations between morphology, chemical types of amyloid protein and clinical features.

Sixty-one autopsy cases of renal amyloidosis were reviewed to assess the relationship of renal pathology to chemical types of amyloid and clinical features. Glomerular amyloid deposition was divided on the basis of morphological characteristics, into four types: a mesangial nodular type showing nodular mesangial deposits with sparse capillary wall involvement (25 cases), a mesangio-capillary type disclosing diffuse amyloid deposition in the mesangium and along both sides of the glomerular basement membrane (19 cases), a perimembranous type principally involving the subepithelial side of the basement membrane invariably characterized by exuberant spicular arrangement (6 cases), and a hilar type showing amyloid deposits almost exclusively in hilar arterioles (11 cases). Twenty-four of 25 cases of mesangial nodular type (96%) showed amyloid protein of AA type. However, mesangio-capillary and perimembranous types were associated with deposition of AL amyloid protein in 15 of 19 (79%) and all 6 cases, respectively. Nephrotic syndrome was more frequent in patients with AL amyloidosis; notably, all patients with perimembranous type had nephrotic syndrome irrespective of the extent of glomerular amyloid deposits. Chronic renal failure and renal death appeared more common in mesangial nodular type in which the extent of glomerular amyloidosis correlated with that of vascular amyloid deposits. The results obtained suggest that the chemical type of glomerular amyloid protein (AA vs AL) is associated with significant differences in the morphological, clinical and prognostic features of the renal involvement.

Adult↗
PubMed1988

Incidence and characterization of age related amyloid deposits in the human anterior pituitary gland.

To identify amyloid deposits in the anterior pituitary gland, we have immunohistochemical, histochemical and alkaline Congo red staining. The anti-human P component reacted positively with these amyloid deposits, while antisera against prealbumin, AA type amyloid fibril protein and various anterior pituitary hormones were negative. A combination of Congo red and anti-human P component staining was most sensitive and reliable for detection of amyloid in the anterior pituitary glands of 300 randomly autopsied patients. Amyloid deposits increased in parallel with the age of the patients, however, they appeared earlier and more frequently than heretofore reported. Deposition of amyloid was seen initially in the 3rd decade and the positivity rate of amyloid deposits was 73% in the 5th decade. The histochemical characteristics of these pituitary amyloid deposits differed from those of cerebral and systemic deposits, particularly those found in the amyloid of senile systemic amyloidosis.

Adolescent↗
PubMed1988

Aging and cerebral amyloid: early detection of amyloid in the human brain using biochemical extraction and immunostain.

To search for relationships between aging and cerebral amyloid, the brains of 66 clinically nondemented individuals were investigated, using the following three approaches for verification of the amyloid: Congo red staining as a histochemical method; immunostaining using anti-beta protein antiserum as an immunohistochemical identification; and biochemical extraction of amyloid from nonfixed brain tissues. That the incidence of cerebral amyloid increased with aging was determined using all three approaches. Immunostaining using anti-beta protein antiserum was more sensitive than Congo red staining. The biochemical extraction was most sensitive for detection of amyloid, and revealed that amyloid was extracted initially from more than half (67%) of the brains of 9 persons in their 50s and from almost all (97%) brains of 35 persons over 60 years of age. Amyloid was extracted even from brains in which amyloid deposits were not detected by histochemical or immunohistochemical methods. This result shows early appearance of the age-related cerebral amyloid.

Aging↗
PubMed1988

Choroid plexus papillomas: an immunohistochemical study with particular reference to the coexpression of prealbumin.

Immunocytochemical characterization of choroid plexus neoplasms was performed in seven cases, five being of benign choroid plexus papilloma (CPP) and the other two of malignant choroid plexus papilloma (choroid plexus carcinoma CPC). Immunohistochemical examination was performed with antibodies to glial fibrillary acidic protein (GFAP), S-100 protein, prealbumin, carcinoembryonic antigen (CEA), epithelial membrane antigen (EMA), and gamma-enolase. All of the five CPPs were positive for GFAP, S-100, prealbumin, and gamma-enolase; and four of them were positive for EMA. None of the CPPs was positive for CEA. Both of the two cases of CPC were positive for gamma-enolase, and one was positive for GFAP, S-100, EMA, and CEA. No CPC showed positivity for prealbumin. This report is the first to describe the usefulness of prealbumin reactivity for histological diagnosis of choroid plexus papillomas.

Adolescent↗
PubMed1988

Immunohistochemical confirmation of Creutzfeldt-Jakob disease with a long clinical course with amyloid plaque core antibodies.

Amyloid plaques have been found in the brains of some patients with Creutzfeldt-Jakob disease (CJD) and all patients with Gerstmann-Sträussler syndrome (GSS). We examined paraffin sections from 45 patients with CJD or GSS and from 51 patients with other neurologic diseases, using an antiserum against GSS amyloid plaque cores. The GSS amyloid plaque core antiserum revealed not only birefringent amyloid plaques but also small plaques that cannot be detected by the staining with Congo red dye. Positive immunolabeling was demonstrated in 59% of 34 Japanese patients with CJD, in 100% of 11 patients with GSS, and in none with other neurologic diseases. All cases of CJD of short duration (less than 11 months) were evaluated as being negative, and 95% of 21 long survivors (over 12 months) were positive. This immunohistochemical approach revealed that amyloid plaque is a hallmark of CJD with a long clinical course.

Amyloid↗
PubMed1987

Choroidal epithelial cyst of the cerebral hemisphere. An immunohistochemical study.

A case of choroidal epithelial cyst in the left cerebral hemisphere of a 4-month-old infant is described. The cyst wall was composed of a single epithelial layer with a basement membrane and fibrous connective tissue. An immunohistochemical study revealed the presence of prealbumin in the cytoplasm of these cuboidal epithelial cells. This fact strongly suggested that the cuboidal epithelium lining the cyst wall originated from choroidal epithelial cells. The diagnostic usefulness of the immunohistochemical study in choroidal epithelial cysts is discussed.

Choroid Plexus↗
PubMed1987

Formic acid pretreatment enhances immunostaining of cerebral and systemic amyloids.

The purpose of this study was to design a method by which immunoperoxidase staining can be applied to formalin-fixed, paraffin-embedded tissue sections to demonstrate amyloid deposits in cerebral and systemic amyloidotic tissues. We used anti-prion protein, anti-beta-protein, anti-amyloid A, and anti-prealbumin antisera. The tissue sections were first treated with 100% formic acid for 5, 20, or 60 minutes and the unlabeled immunoperoxidase method (biotin-streptavidin system reagents) was used. This formic acid pretreatment enhanced immunoreactivity of the amyloid deposits which reacted positively with specific antiserum. The specificity of the immunostainings was well preserved. This method can also be used to demonstrate interspecies cross-reactivity, by using anti-human amyloid A and anti-scrapie hamster prion protein antisera, which stained negatively or faintly with amyloid deposits of heterogenous species. The technique is expected to reveal the buried epitopes of amyloid deposits in tissue sections.

Alzheimer Disease↗
PubMed1986

Congophilia in cerebral amyloidosis is modified by inactivation procedures on slow transmissible pathogens.

Cerebral tissues with amyloid deposits were treated by various chemicals which inactivated the agent of subacute spongiform encephalopathy (SSE). We discovered Congophilia in the amyloid plaques in cases of Creutzfeldt-Jakob disease (CJD) and Gerstmann-Sträussler syndrome (GSS) correlated to the chemical inactivation profiles of SSE. After incubation with trichloroacetate, guanidine-SCN, guanidine-HCl, formic acid, phenol and autoclaving, amyloid plaques in unfixed frozen sections of human brains with CJD or GSS, lost the affinity of Congo red and green birefringence under polarized light. In formalin-fixed, paraffin-embedded tissue sections, amyloid plaques of CJD and GSS lost the affinity of Congo red after most of these treatments. On the other hand, senile plaques in the aged, patients with Alzheimer's disease and with senile dementia of the Alzheimer type did not lose the affinity of Congo red after most of these treatments. Therefore, the amyloid deposits in the amyloid plaques differ from those in senile plaques. The methods we used facilitate differentiation of amyloid and senile plaques in formalin-fixed, paraffin-embedded tissues.

Alzheimer Disease↗
PubMed1986

Nonfamilial prealbumin-type amyloid polyneuropathy.

A 53-year-old man with nonfamilial prealbumin-type amyloid polyneuropathy had severe motor, sensory, and autonomic polyneuropathy, beginning at age 48 years. These clinical features closely resembled familial amyloid polyneuropathy (FAP), but abnormal serum prealbumin levels, specific to FAP (Japanese type), were not detected by radioimmunoassay; DNA sequence for prealbumin was normal. Thus, the diagnosis of FAP was excluded. A possible diagnosis of systemic senile amyloidosis was also considered.

Amyloidosis↗
PubMed1986

Amyloid plaques in Creutzfeldt-Jakob disease stain with prion protein antibodies.

Amyloid plaques are found in the brains of some patients with Creutzfeldt-Jakob disease (CJD) and all patients with a related transmissible disorder, Gerstmann-Sträussler syndrome (GSS). In scrapie, a prion disease of animals, amyloid plaques have been shown to be composed of prion proteins (PrP), which form filaments of relatively uniform diameter. We report here that antisera raised against hamster scrapie PrP specifically stain amyloid plaques in the brains of both humans and rodents with CJD as well as a human subject with GSS. Earlier studies showed that these antibodies react with both rodent and human CJD PrP. The immunostained congophilic amyloid plaques in rodent brains measured 10 to 30 micron in diameter and exhibited a Maltese cross appearance. Limited proteolysis enhanced immunostaining of amyloid plaques in human brain sections from patients with CJD or GSS. Presumably proteolysis increases the exposure of those epitopes shared by human and rodent PrP. The differences in immunoreactivity between rodent and human amyloid plaques are consistent with other findings showing that cellular genes, not infectious purified prions, encode PrP.

Amyloid↗
PubMed1986

Scrapie-associated fibrils (SAF) purification method yields amyloid proteins from systemic and cerebral amyloidosis.

We identified fibrils from non-transmissible systemic and cerebral amyloidosis using the purification method of scrapie-associated fibrils (SAF). The fibrils possessed the same nature of congophilia, filamentous structures and molecular weights as amyloid fibrils, and were resistant to Proteinase K digestion. This SAF method makes for a rapid extraction from amyloid-laden tissues. The method, therefore, may purify nontransmissible amyloids alone or together with SAF proteins.

Amyloid↗
PubMed1986

Histochemical classification of systemic amyloid fibril proteins. Alkaline guanidine method.

The alkaline guanidine method facilitates differentiation between different types of amyloid fibril proteins in formaldehyde-fixed, paraffin-embedded tissue sections. Systemic AA-type amyloids lost Congophilia (affinity of Congo red) after incubation with alkaline guanidine for one minute. Systemic AL-type amyloids lost or markedly decreased Congophilia after two hours of treatment with alkaline guanidine. Systemic prealbumin-type amyloids were resistant to incubation for two hours. On the other hand, some cerebral amyloid plaques from patients with Creutzfeldt-Jakob disease and Gerstmann-Sträussler syndrome markedly decreased Congophilia, while in other amyloid plaques, Congophilia was not decreased even with two hours of treatment. The senile plaques from those patients with Alzheimer's disease did not diminish Congophilia after alkaline guanidine treatment. Thus, while this method does not differentiate types of cerebral amyloid protein, it does clearly differentiate types of systemic amyloid fibril proteins.

Adolescent↗