Does transnasal delivery of human A-beta peptides elicit impaired learning and memory performance in wild type mice?
Existing AD mouse models are of genetic origin and need prolonged housing time before onset of pathology. Our short-term treatment induced learning and memory deficits via exogenous application of A-beta peptides comparable to those observed for the transgenic animals. With the transnasal A-beta 42 treatment we present an approach to investigate purely A-beta related changes suitable as a model for symptoms of Alzheimer's dementia (AD). Resulting behavioral deficits were indicative for familial type of Alzheimer's disease as well as for the late onset variant.
These observations suggest modulation of TGF-beta1 expression as a novel mechanism of salutary effect of NO donors. PKC-alpha activation may play an important role in the protective effect of NO against H-R injury.