Alzheimer hastalığı’nda gözlenen senil plakların immunohistokimyasal metodlarla gösterilmesi
Küçük Resim Yok
Tarih
2001
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Ankara Patoloji Derneği
Erişim Hakkı
CC0 1.0 Universal
info:eu-repo/semantics/openAccess
info:eu-repo/semantics/openAccess
Özet
Son yıllarda; Alzheimer hastalığının etiyolojisi, patogenezi, erken tanı ve tedavisi konusunda çok sayıda çalışma yapılmaktadır. Alzheimer hastalığı'nda izlenen başlıca histopatolojik bulguların; "nörofibril yumaklar, senil (nörotik) plaklar, kongofil anjiopati, granülovasküler dejenerasyon ve Hirano cisimcikleri" olduğu bildirilmiştir 1. Bunlardan senil plaklar; beyinde nöronal kayıp, nörofibriler dejenerasyon ve ekstrasellüler amiloid birikimine bağlı olarak oluşan lezyonlardır 2. Alzheimer hastalığı dışında; fizyolojik yaşlılıkta, Kuru, Creutzfeld Jakob ve Down sendromunda da görülmektedir 1,3. Tipik bir senil plak; Aluminyum ve silikat içeren amorf bir kor ile çevresindeki anormal şişmiş akson ve dendritik elemanlar, glial uzantılar, astrositler ve nörofibril yumaklarından oluşan gevşek yapıda bir kısımdan meydana gelir. Yapılan araştırmalar; senil plakların farklı tiplerdeki amiloid proteinleri, Tau proteini, alpha-1-antikimotripsin, apolipoprotein E ve ubiquitin içerdiğini göstermiştir 3-12. Senil plakların içerdiği amiloidin en yaygın formunun "b-amiloid" olduğu bildirilmiştir 2,4,7-11,13. "Tau" ise; matür plaklarda bulunan ve şişmiş nöritlerde saptanan bir diğer proteindir 2,12,14. Çalışmamızda, hastalığın farklı klinik dönemlerinde senil plaklarda meydana gelen beta-amiloid ve Tau birikimini karşılaştırmalı olarak immunohistokimyasal yöntemlerle göstermeyi amaçladık.
The aim of the study was to demonstrate the accumulation of b-amiloid and Tau in different clinical stages of Alzheimer's disease by using immunohistochemical methods. Primates, having Alzheimer's disease experimentally, were grouped into four clinical stages: Early confusion, late confusion, early demans and late demans. After perfusion of paraformaldehit %1/glutaraldehit %4, specimens from their cerebral cortex were embedded in paraffin. The sections were immunostained with anti-beta-amiloid and anti-Tau by using avidin-biotin-peroxidase staining technique. There was significant staining with beta-amiloid from the begining of the disease to the end. The method has demonstrated that senile plaques increase in number and size while the immunostaining becomes significantly intense according to the clinical stage of Alzheimer's disease. The immunoreactivity for Tau in senile plaques was quite similar in early stages and the staining intensity was lighter than the staining for b-amiloid. Immunostaining for "Tau" protein became more significant and senile plaques could be demonstrated at the late stage of demans. These results show that there is significant accumulation of beta-Amiloid from the beginning of Alzheimer's disease to the end; while Tau accumulation becomes more intense at the late stages of the disease. Immunohistochemical demonstration of beta-Amiloid might help to demonstrate the existence of senile plaques from the beginning of the disease while Tau can be detected at the later stages of Alzheimer's disease.
The aim of the study was to demonstrate the accumulation of b-amiloid and Tau in different clinical stages of Alzheimer's disease by using immunohistochemical methods. Primates, having Alzheimer's disease experimentally, were grouped into four clinical stages: Early confusion, late confusion, early demans and late demans. After perfusion of paraformaldehit %1/glutaraldehit %4, specimens from their cerebral cortex were embedded in paraffin. The sections were immunostained with anti-beta-amiloid and anti-Tau by using avidin-biotin-peroxidase staining technique. There was significant staining with beta-amiloid from the begining of the disease to the end. The method has demonstrated that senile plaques increase in number and size while the immunostaining becomes significantly intense according to the clinical stage of Alzheimer's disease. The immunoreactivity for Tau in senile plaques was quite similar in early stages and the staining intensity was lighter than the staining for b-amiloid. Immunostaining for "Tau" protein became more significant and senile plaques could be demonstrated at the late stage of demans. These results show that there is significant accumulation of beta-Amiloid from the beginning of Alzheimer's disease to the end; while Tau accumulation becomes more intense at the late stages of the disease. Immunohistochemical demonstration of beta-Amiloid might help to demonstrate the existence of senile plaques from the beginning of the disease while Tau can be detected at the later stages of Alzheimer's disease.
Açıklama
Anahtar Kelimeler
Kaynak
Patoloji Bülteni
WoS Q Değeri
Scopus Q Değeri
Cilt
18
Sayı
1
Künye
Aktaş, R. G. ve Kayton, R. J. (2001). Alzheimer hastalığı’nda gözlenen senil plakların immunohistokimyasal metodlarla gösterilmesi / Immunohistochemical demonstration of senile plaques in Alzheimer’s disease. Patoloji Bülteni, Ankara Patoloji Derneği. 18(1), s. 35-38.
