Please use this identifier to cite or link to this item:
http://dspace.mediu.edu.my:8181/xmlui/handle/123456789/4049| Title: | Amyloid beta protein restores hippocampal long term potentiation: a central role for cholesterol? |
| Keywords: | Alzheimer's disease amyloid precursor protein APP Down syndrome etiology lipids learning memory long-term potentiation LTP LRP neurodegeneration oxidative stress anti oxidation PHF NFT tau plaques phospholipids secretase synapse synaptic plasticity SREBP statins Liver X LXR sensor presenilin |
| Issue Date: | 30-May-2013 |
| Publisher: | Neurobiology of Lipids |
| Description: | There is no understanding of the role of amyloid beta protein (Ab or Abeta) in brain function and Alzheimer's disease. In the present study we attempted to dissect out the role for Abeta in the synaptic plasticity in adult rat ex vivo hippocampal slices. The prolonged incubation of slices in our experimental setting preserved basic synaptic physiology but abrogated tetanus induced long term potentiation (LTP). Peptide Abeta1-40 rescued LTP while cholesterol synthesis inhibition abolished the restorative action of the peptide. Our observation confirms that Abeta protein is a functional player in cholesterol neurochemical pathways and in synaptic structure-functional plasticity. The finding also supports our proposed hypothesis that the change in Abeta biochemistry in Alzheimer's disease is a functional phenomenon aiming to compensate impaired cholesterol dynamics and associated neurotransmission and synaptic plasticity failure. |
| URI: | http://koha.mediu.edu.my:8181/jspui/handle/123456789/4049 |
| Other Identifiers: | http://neurobiologyoflipids.org/content/1/8/ http://www.doaj.org/doaj?func=openurl&genre=article&issn=16835506&date=2003&volume=1&issue=&spage=46 |
| Appears in Collections: | Biology and Life Sciences |
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.