Faculty Opinions recommendation of Attenuation of neuroinflammation and Alzheimer's disease pathology by liver x receptors.

Author(s):  
Ernest Arenas
2007 ◽  
Vol 104 (25) ◽  
pp. 10601-10606 ◽  
Author(s):  
N. Zelcer ◽  
N. Khanlou ◽  
R. Clare ◽  
Q. Jiang ◽  
E. G. Reed-Geaghan ◽  
...  

2013 ◽  
Vol 4 (3) ◽  
Author(s):  
Jasminka Štefulj ◽  
Ute Panzenboeck ◽  
Patrick Hof ◽  
Goran Šimić

AbstractThe pathogenesis of Alzheimer’s disease (AD) has been mostly linked to aberrant amyloid beta (Aβ) and tau proteins metabolism, disturbed lipid/cholesterol homeostasis, and progressive neuroinflammation. Liver X receptors (LXR) are ligand-activated transcription factors, best known as the key regulators of cholesterol metabolism and transport. In addition, LXR signaling has been shown to have significant anti-inflammatory properties. In this brief review, we focus on the outcome of studies implicating LXR in the pathogenesis, modulation, and therapy of AD.


2012 ◽  
Vol 33 (5) ◽  
pp. 715-746 ◽  
Author(s):  
Jihong Kang ◽  
Serge Rivest

Liver X receptors (LXR) are nuclear receptors that have emerged as key regulators of lipid metabolism. In addition to their functions as cholesterol sensors, LXR have also been found to regulate inflammatory responses in macrophages. Alzheimer's disease (AD) is a neurodegenerative disease characterized by a progressive cognitive decline associated with inflammation. Evidence indicates that the initiation and progression of AD is linked to aberrant cholesterol metabolism and inflammation. Activation of LXR can regulate neuroinflammation and decrease amyloid-β peptide accumulation. Here, we highlight the role of LXR in orchestrating lipid homeostasis and neuroinflammation in the brain. In addition, diabetes mellitus is also briefly discussed as a significant risk factor for AD because of the appearing beneficial effects of LXR on glucose homeostasis. The ability of LXR to attenuate AD pathology makes them potential therapeutic targets for this neurodegenerative disease.


2019 ◽  
Vol 176 (18) ◽  
pp. 3599-3610 ◽  
Author(s):  
Nicholas F. Fitz ◽  
Kyong Nyon Nam ◽  
Radosveta Koldamova ◽  
Iliya Lefterov

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.


Author(s):  
J. Metuzals ◽  
D. F. Clapin ◽  
V. Montpetit

Information on the conformation of paired helical filaments (PHF) and the neurofilamentous (NF) network is essential for an understanding of the mechanisms involved in the formation of the primary lesions of Alzheimer's disease (AD): tangles and plaques. The structural and chemical relationships between the NF and the PHF have to be clarified in order to discover the etiological factors of this disease. We are investigating by stereo electron microscopic and biochemical techniques frontal lobe biopsies from patients with AD and squid giant axon preparations. The helical nature of the lesion in AD is related to pathological alterations of basic properties of the nervous system due to the helical symmetry that exists at all hierarchic structural levels in the normal brain. Because of this helical symmetry of NF protein assemblies and PHF, the employment of structure reconstruction techniques to determine the conformation, particularly the handedness of these structures, is most promising. Figs. 1-3 are frontal lobe biopsies.


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