Neurofibromatosis 1 (NF1) is a common single-gene disorder that causes learning 
impairments in patients. Neurofibromin encoded by the NF1 causal gene regulates 
Ras/MAPK and cAMP signaling pathways. These signaling pathways play critical 
roles in controlling gene transcription during synaptic plasticity and memory 
formation. We hypothesized that NF1 mutations disturb the expression of genes 
important for memory formation. To test this hypothesis, we performed DNA 
microarray analysis on the hippocampus of NF1(+/-) mice, the mouse model for NF1 
learning disabilities. Our results indicated that genes involved in a wide 
spectrum of biological processes are dysregulated in the NF1(+/-) hippocampus. 
Many of the NF1-affected genes play critical roles in synaptic plasticity, such 
as Rabs, synaptotagmins, NMDAR1, CaMKII, and CREB1. Because NF1-associated 
learning disabilities can be reversed by lovastatin, we also determined the 
effect of lovastatin treatment on genome-wide expression patterns of the 
NF1(+/-) hippocampus. We found that lovastatin altered the expression of a large 
number of genes, including those disturbed by NF1 mutations. Our results reveal 
a genome-wide overview of the molecular abnormalities in the NF1(+/-) 
hippocampus and should be useful for further identifying the novel molecular 
pathways that cause NF1 learning deficits.