Article
p75 reduces beta-amyloid-induced sympathetic innervation deficits in an Alzheimer's disease mouse model.
Proceedings of the National Academy of Sciences of the United States of America - 12 May 2009
Bengoechea Tasha G, Chen Zhijiang, O'Leary Debra A, O'Leary Deborah, Masliah Eliezer, Lee Kuo-Fen
Abstract excerpt
Beta-amyloid (Abeta) has adverse effects on brain cells, but little is known about its effects on the peripheral nervous system in Alzheimer's disease (AD). Several lines of in vitro evidence suggest that the neurotrophin receptor p75 mediates or exacerbates Abeta-induced neurotoxicity. Here, we show that p75-deficient sympathetic neurons are more sensitive to Abeta-induced neurite growth inhibition. To...
Topics
- Alzheimer Disease
- Amyloid Precursor Protein Secretases
- Amyloid beta-Peptides
- Animals
- Aspartic Acid Endopeptidases
- Disease Models, Animal
- Male
- Mice
- Mice, Transgenic
- Mutation
- Neurons
- Receptor, Nerve Growth Factor
- Stellate Ganglion