PMCC PMCC

Search tips
Search criteria

Advanced
Results 1-2 (2)
 

Clipboard (0)
None

Select a Filter Below

Journals
Authors
Year of Publication
Document Types
1.  Regulation of CREB and hippocampal plasticity-related genes by peroxisome proliferator-activated receptor α 
Cell reports  2013;4(4):724-737.
Peroxisome proliferator-activated receptor (PPAR) α is a transcription factor that regulates genes involved in fatty acid catabolism. Here we provide evidence that PPARα is constitutively expressed in nuclei of hippocampal neurons and surprisingly controls calcium influx and the expression of various plasticity-related genes via direct transcriptional regulation of CREB. Accordingly, Ppara-null, but not Pparb-null, mice are deficient in CREB and memory-associated genes, and have decreased spatial learning and memory. While shRNA knockdown of PPARα in the hippocampus suppressed CREB and NR2A rendering wild type animals markedly poor in consolidating spatial memory, introduction of PPARα to the hippocampus of Ppara-null mice increased hippocampal CREB and NR2A and improved spatial learning and memory. These results together with detailed analyses of CREB, NR2A and spatial learning and memory in bone marrow chimeric animals lacking PPARα in the CNS describe a novel mechanism for transcriptional control of Creb and associated plasticity genes by PPARα.
doi:10.1016/j.celrep.2013.07.028
PMCID: PMC3804033  PMID: 23972989
2.  Trophic factors therapy in Parkinson’s disease 
Progress in brain research  2009;175:201-216.
Parkinson’s disease (PD) is a progressive, neurodegenerative disorder for which there is currently no effective neuroprotective therapy. Patients are typically treated with a combination of drug therapies and/or receive deep brain stimulation to combat behavioral symptoms. The ideal candidate therapy would be the one which prevents neurodegeneration in the brain, thereby halting the progression of debilitating disease symptoms. Neurotrophic factors have been in the forefront of PD research, and clinical trials have been initiated using members of the GDNF family of ligands (GFLs). GFLs have been shown to be trophic to ventral mesencephalic cells, thereby making them good candidates for PD research. This paper examines the use of GDNF and neurturin, two members of the GFL, in both animal models of PD and clinical trials.
doi:10.1016/S0079-6123(09)17514-3
PMCID: PMC3430519  PMID: 19660658
neurotrophic factors; Parkinson’s disease; glial cell line-derived neurotrophic factor family ligands; GDNF; neurturin; gene therapy; clinical trials

Results 1-2 (2)