Alzheimer disease (AD) is a neurodegenerative pathology mainly associated with amyloid-Î² (AÎ²) peptide aggregation and deposition in brain parenchyma and perivascular spaces. This hallmark results from altered natural processes of clearance of these peptides from brain. Finding a treatment for AD has become the main challenge of the 21st century for the scientific community due to the progressive increase of people affected and the rising costs of care. Since the last decade, a new promising therapeutical strategy based on the stimulation of liver X receptors (LXRs) by agonists has arisen to slow down the evolution of AD. LXRs are ligand-activated transcription factors which are involved in cellular cholesterol metabolism by regulating the expression of target genes. These nuclear receptors have been linked with the onset and progression of AD since APP/PS1 mice deficient for LXRs showed a greater number of AÎ² plaques in brain parenchyma and an accelerated cognitive decline. The close relationship between LXRs and AD is associated with the transporter ATP Binding Cassette sub-family A member 1 (ABCA1) which regulate the cerebral cholesterol release to apolipoprotein E (ApoE). Indeed, ABCA1 depletion in AD-related mice models led to an increased deposition of AÎ² peptides in brain where as it is over expression reduced the cerebral AÎ² burden.
The LXR/RXR Approaches in Alzheimerâs Disease: Is the Blood-Bra in Barrier the Forgotten Partner?- Fabien Gosselet
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Last date updated on June, 2014