Premium
[P‐098]: Amyloid deposits imaging by passive staining in mouse models of Alzheimer's disease
Author(s) -
Dhenain Marc,
Volk Andreas,
Walczak Christine,
Delatour Benoit
Publication year - 2005
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2005.06.172
Subject(s) - staining , pathology , vibratome , chemistry , amyloid (mycology) , gadolinium , senile plaques , cerebral amyloid angiopathy , contrast (vision) , nuclear medicine , alzheimer's disease , medicine , immunohistochemistry , dementia , organic chemistry , artificial intelligence , computer science , disease
A 1-42). Conclusions: Compact neuritic A plaques were abundant in the frontal cortex and absent in the cerebellum. 6-CN-BTA-1 bound to blood vessels and A 1-16/tau dual-labeled compact neuritic plaques in the frontal cortex; binding was not detected in the cerebellum. 6-CN-BTA-1 was more readily detected in A 1-40-immunoreactive (ir) plaques than in A 1-42-ir plaques. Diffuse non-neuritic A deposits were devoid of 6-CN-BTA-1 staining. Pretreatment of tissue sections with formic acid completely abolished 6-CN-BTA-1 staining. Our results demonstrate that 6-CN-BTA-1 labels preferentially compact neuritic plaques in AD brain, suggesting its affinity for binding to aggregated A . These data aid in interpreting the binding properties of the parent compound of 6-CN-BTA-1, PIB, which is currently under evaluation as an in vivo diagnostic marker of diseasespecific A plaque pathology progression in AD brains.