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Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Cognitive deficits are ameliorated by reduction in amyloid β accumulation in Tg2576/p75(NTR+/-) mice
Chongdong Jian1, Donghua Zou2, Chun Luo2
1Guangxi Medical University, No. 22 Shuangyong Road, Nanning, Guangxi 530021, China; Affiliated Hospital of Youjiang Medical University for Nationalities, No. 18 Zhongshan Er Road, Baise, Guangxi 533000, China.
Aims:
Amyloid β (Aβ) is considered to be an important mediator of the development and progression of Alzheimer's disease (AD). Its direct binding to p75(NTR), not TrkA, induces apoptosis, which is thought to be the most relevant feature of p75(NTR) regarding AD. In the present study we explored the regulation of p75(NTR) on Aβ production and accumulation during AD pathology.
Materials And Methods:
We generated Tg2576/p75(NTR+/-) mice by crossing the transgenic AD mice (Tg2576) with p75(NTR-/-) mice to lower the p75(NTR) level. Under these conditions, we evaluated cognitive function using the Morris water maze, pathology and process by which two types of Aβ (Aβ40 and Aβ42) are produced, by enzyme-linked immunosorbent assay and Western blotting.
Key Finding:
The results showed that cognitive deficits were rescued in Tg2576/p75(NTR+/-) mice compared with those in Tg2576 mice. This cognitive functional recovery may be a consequence of a reduction in Aβ accumulation through the inhibition of β- and γ-secretase activities, without altering α-secretase activity.
Significance:
Here, we investigated the mechanism by which p75(NTR) regulates Aβ production and accumulation. Better understanding the relationship between p75(NTR) and Aβ producing may help taking insight into the AD pathology.
