Abstract：
:We have shown that, when an amyloid-beta peptide (Abeta) overproducing transgenic mouse model (PSAPP) of Alzheimer's disease (AD) is treated with a depleting antibody against CD40L, it causes marked attenuation of Abeta pathology associated with decreased amyloidogenic processing of amyloid precursor protein (APP) and increased cerebral clearance of Abeta. Here, we report that, when PSAPP mice receive a regimen of anti-CD40L antibody commencing at an age associated with initial Abeta deposition, they demonstrate superior spatial memory on the standard water maze and radial arm water maze tasks, as well as exhibiting superior non-spatial memory in the object recognition test, as compared to control PSAPP mice. Furthermore, PSAPP mice treated with an anti-CD40L antibody regimen commencing at an age associated with extensive Abeta deposition demonstrate superior spatial memory on the standard water maze task, as compared to control PSAPP mice. Disruption of CD40L activity has beneficial effects on pathology and cognitive behavior in the PSAPP mouse model, providing support for the therapeutic potential of interrupting the CD40-CD40L interaction in AD.
journal_name
Brain Resjournal_title
Brain researchauthors
Todd Roach J,Volmar CH,Dwivedi S,Town T,Crescentini R,Crawford F,Tan J,Mullan Mdoi
10.1016/j.brainres.2004.05.004subject
Has Abstractpub_date
2004-07-23 00:00:00pages
161-8issue
1-2eissn
0006-8993issn
1872-6240pii
S0006899304007255journal_volume
1015pub_type
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