Reduction of p75 neurotrophin receptor ameliorates the cognitive deficits in a model of Alzheimer's disease.

Abstract

Alzheimer's disease (AD) is an extremely prevalent cause of dementia. It is characterized by progressive memory loss, confusion, and other behavioral and physiological problems. The amyloid-β (Aβ) protein is thought to be involved in the pathogenesis of AD, and there is evidence that Aβ may act through the p75 neurotrophin receptor (p75) to mediate its pathogenic effects. This raises the possibility that reducing levels of p75 could be a treatment for AD by preventing the effects of Aβ. In this study, we have crossed the transgenic AD model mice, Tg2576, with p75(-/-) mice to generate Tg2576/p75(+/-) mice with reduced levels of p75. These mice are rescued from the deficits in learning and memory and hippocampal function which were found in the Tg2576 mice. These findings suggest that reduction of p75 can ameliorate some of the primary symptoms of AD.

• Authors: Mark Murphy, Yvette M Wilson, Ernesto Vargas, Kathryn M Munro, Belinda Smith, Amy Huang, Qiao-Xin Li, Junhua Xiao, Colin L Masters, Christopher A Reid, Graham L Barrett
• Journal: Neurobiology of aging (Neurobiol Aging) Vol. 36 Issue 2 Pg. 740-52 (Feb 2015) ISSN: 1558-1497 [Electronic] United States
• PMID: 25443284 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Crown Copyright © 2015. Published by Elsevier Inc. All rights reserved.

Chemical References

• Amyloid beta-Peptides
• Receptors, Nerve Growth Factor
• TNFRSF16 protein, mouse

Topics

• Alzheimer Disease (genetics, metabolism, physiopathology, psychology)
• Amyloid beta-Peptides (metabolism)
• Animals
• Disease Models, Animal
• Female
• Hippocampus (physiopathology)
• Humans
• Learning
• Male
• Memory
• Mice, Transgenic
• Receptors, Nerve Growth Factor (metabolism, physiology)