Stimulation of endogenous neurogenesis by anti-EFRH immunization in a transgenic mouse model of Alzheimer's disease.
Ontology highlight
ABSTRACT: Neurogenesis is a subject of intense interest and extensive research, but it stands at the center of a bitter debate over ethical and practical problems. Neurodegenerative diseases, such as Alzheimer's disease (AD), accompanied by a shifting balance between neurogenesis and neurodegeneration, are suitable for stimulation of neurogenesis for the benefit of diseased patients. We have previously shown that Abs against the EFRH sequence of beta-amyloid peptide (AbetaP) prevent aggregation and disaggregate AbetaP both in vitro and in vivo. EFRH, located in the soluble tail of the N-terminal region, acts as a regulatory site controlling both solubilization and disaggregation processes in the AbetaP molecule. Here we show that anti-EFRH immunotherapy of a platelet-derived amyloid precursor protei
SUBMITTER: Becker M
PROVIDER: S-EPMC1785268 | biostudies-literature | 2007 Jan
REPOSITORIES: biostudies-literature
ACCESS DATA