Pharmacological activation of the nuclear receptor REV-ERB reverses cognitive deficits and reduces amyloid-β burden in a mouse model of Alzheimer's disease

Alzheimer's disease currently lacks treatment options that effectively reverse the biological/anatomical pathology and cognitive deficits associated with the disease. Loss of function of the nuclear receptor REV-ERB is associated with reduced cognitive function in mouse models. The effect of en...

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Veröffentlicht in:	PloS one 2019-04, Vol.14 (4), p.e0215004
Hauptverfasser:	Roby, Deborah A, Ruiz, Fernanda, Kermath, Bailey A, Voorhees, Jaymie R, Niehoff, Michael, Zhang, Jinsong, Morley, John E, Musiek, Erik S, Farr, Susan A, Burris, Thomas P
Format:	Artikel
Sprache:	eng
Schlagworte:	Alzheimer Disease - drug therapy Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - metabolism Animal cognition Animal models Animals Biological effects Biology and Life Sciences Circadian rhythm Cognitive ability Cognitive Dysfunction - drug therapy Cognitive Dysfunction - metabolism Cognitive Dysfunction - pathology Cortex Disease Models, Animal Disks Large Homolog 4 Protein - metabolism Footshock Gene expression Genetic engineering Hippocampus Hippocampus - metabolism Hippocampus - pathology Internal medicine Laboratory animals Ligands Male Medical treatment Medicine Medicine and Health Sciences Memory Mice Nuclear Receptor Subfamily 1, Group D, Member 1 - metabolism Object recognition Operant conditioning Pattern recognition Peptide Fragments - metabolism Pharmacology Pharmacy Physiology Postsynaptic density proteins Pyrrolidines - pharmacology Research and Analysis Methods Synapses Synaptophysin Thiophenes - pharmacology
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