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Evidence of amyloid β-protein immunoreactive early plaque lesions in Down's syndrome brains

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Evidence of amyloid β-protein immunoreactive early plaque lesions in Down's syndrome brains. / Ikeda, S; Yanagisawa, N; Allsop, D et al.
In: Laboratory Investigation, Vol. 61, No. 1, 1989, p. 133-137.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Ikeda, S, Yanagisawa, N, Allsop, D & Glenner, GG 1989, 'Evidence of amyloid β-protein immunoreactive early plaque lesions in Down's syndrome brains', Laboratory Investigation, vol. 61, no. 1, pp. 133-137.

APA

Ikeda, S., Yanagisawa, N., Allsop, D., & Glenner, G. G. (1989). Evidence of amyloid β-protein immunoreactive early plaque lesions in Down's syndrome brains. Laboratory Investigation, 61(1), 133-137.

Vancouver

Ikeda S, Yanagisawa N, Allsop D, Glenner GG. Evidence of amyloid β-protein immunoreactive early plaque lesions in Down's syndrome brains. Laboratory Investigation. 1989;61(1):133-137.

Author

Ikeda, S ; Yanagisawa, N ; Allsop, D et al. / Evidence of amyloid β-protein immunoreactive early plaque lesions in Down's syndrome brains. In: Laboratory Investigation. 1989 ; Vol. 61, No. 1. pp. 133-137.

Bibtex

@article{72ca2130d4d3442ba46b101adf4655e5,
title = "Evidence of amyloid β-protein immunoreactive early plaque lesions in Down's syndrome brains",
abstract = "An immunohistochemical study was carried out on the brains of 12 cases with Down's syndrome (ages 18 to 62) using a monoclonal antibody to amyloid beta-protein with formic acid pretreatment of the sections. Localized ill-defined, weakly immunostained areas with a reticulogranular appearance were the only neocortical lesions observed in two cases aged 31 years. The presence of similar immunoreactive areas with larger size were the predominant cerebral lesions seen in 3 cases who died at the ages of 37 or 38 years. These resembled the {"}type 3{"} immunoreactive lesions (lacking any obvious amyloid deposits or abnormal neurites) that were observed previously by us in Alzheimer's disease. In addition to these lesions, older cases of Down's syndrome over 50 years of age showed discrete senile plaques with substantial deposits of amyloid (the number of these lesions increased with age), and many neurofibrillary tangles and cerebrovascular amyloid deposits were also found in these cases. The present observations support the theory that the type 3 lesions are an early stage in senile plaque formation, and suggest that an extensive appearance of type 3 lesions easily detected by immunostaining with formic acid pretreatment is an early neuropathologic change in Alzheimer's disease.",
keywords = "Adolescent, Adult, Amyloid, Amyloid beta-Peptides, Brain, Congo Red, Down Syndrome, Humans, Immunohistochemistry, Middle Aged, Silver, Staining and Labeling",
author = "S Ikeda and N Yanagisawa and D Allsop and Glenner, {G G}",
year = "1989",
language = "English",
volume = "61",
pages = "133--137",
journal = "Laboratory Investigation",
issn = "0023-6837",
publisher = "Nature Publishing Group",
number = "1",

}

RIS

TY - JOUR

T1 - Evidence of amyloid β-protein immunoreactive early plaque lesions in Down's syndrome brains

AU - Ikeda, S

AU - Yanagisawa, N

AU - Allsop, D

AU - Glenner, G G

PY - 1989

Y1 - 1989

N2 - An immunohistochemical study was carried out on the brains of 12 cases with Down's syndrome (ages 18 to 62) using a monoclonal antibody to amyloid beta-protein with formic acid pretreatment of the sections. Localized ill-defined, weakly immunostained areas with a reticulogranular appearance were the only neocortical lesions observed in two cases aged 31 years. The presence of similar immunoreactive areas with larger size were the predominant cerebral lesions seen in 3 cases who died at the ages of 37 or 38 years. These resembled the "type 3" immunoreactive lesions (lacking any obvious amyloid deposits or abnormal neurites) that were observed previously by us in Alzheimer's disease. In addition to these lesions, older cases of Down's syndrome over 50 years of age showed discrete senile plaques with substantial deposits of amyloid (the number of these lesions increased with age), and many neurofibrillary tangles and cerebrovascular amyloid deposits were also found in these cases. The present observations support the theory that the type 3 lesions are an early stage in senile plaque formation, and suggest that an extensive appearance of type 3 lesions easily detected by immunostaining with formic acid pretreatment is an early neuropathologic change in Alzheimer's disease.

AB - An immunohistochemical study was carried out on the brains of 12 cases with Down's syndrome (ages 18 to 62) using a monoclonal antibody to amyloid beta-protein with formic acid pretreatment of the sections. Localized ill-defined, weakly immunostained areas with a reticulogranular appearance were the only neocortical lesions observed in two cases aged 31 years. The presence of similar immunoreactive areas with larger size were the predominant cerebral lesions seen in 3 cases who died at the ages of 37 or 38 years. These resembled the "type 3" immunoreactive lesions (lacking any obvious amyloid deposits or abnormal neurites) that were observed previously by us in Alzheimer's disease. In addition to these lesions, older cases of Down's syndrome over 50 years of age showed discrete senile plaques with substantial deposits of amyloid (the number of these lesions increased with age), and many neurofibrillary tangles and cerebrovascular amyloid deposits were also found in these cases. The present observations support the theory that the type 3 lesions are an early stage in senile plaque formation, and suggest that an extensive appearance of type 3 lesions easily detected by immunostaining with formic acid pretreatment is an early neuropathologic change in Alzheimer's disease.

KW - Adolescent

KW - Adult

KW - Amyloid

KW - Amyloid beta-Peptides

KW - Brain

KW - Congo Red

KW - Down Syndrome

KW - Humans

KW - Immunohistochemistry

KW - Middle Aged

KW - Silver

KW - Staining and Labeling

M3 - Journal article

C2 - 2473275

VL - 61

SP - 133

EP - 137

JO - Laboratory Investigation

JF - Laboratory Investigation

SN - 0023-6837

IS - 1

ER -