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.