Bulk RNA seq on cerebral cortices derived from WT and Mecp2 null mice (P60) tretaed or not with rhNGF
MECP2 deficiency causes a broad spectrum of neuropsychiatric disorders that can affect both genders, among which Rett syndrome is the most frequent. Main feature of Rett syndrome is an apparent normal development followed by a regression phase in which patients lose most of the previously acquired skills. After this dramatic period, several symptoms progressively get in, including severe intellectual disability, epilepsy, apraxia, breathing abnormalities and motor deterioration. MECP2 codes for an epigenetic transcriptional factor particularly abundant in brain; accordingly, several transcriptional defects characterize the Rett syndrome brain. The well recognized deficiency in different neurotrophins and growth factors in Rett patients and mouse models of Mecp2 deficiency led us to investigate the therapeutic potential of nerve growth factor. The study was performed administrating a GMP-grade recombinant human NGF (rhNGF). To identify  molecular mechanisms triggering the observed benefits an unbiased RNAseq study was performed. Overall design: 6 WT and 6 Mecp2 null mouse male brain cortices (P60) treated or not (control) with rhNGF from P30 to P60. Untreated mice were treated with vehicle (PBS).