Neurofibromatosis type I is a monogenetic disorder resulting from a defective copy of the neurofibromin 1 gene. Patients display a complex and varied clinical presentation which may include frequent tumour formation, hyperpigmentation marks, vision disorders and scoliosis. In addition, learning difficulties and psychiatric conditions such as ADHD, autism, anxiety or depression affect the majority of NF1 patients, and these symptom complexes are not addressed by standard therapeutic strategies. Here we employed a mouse model of NF1, the heterozygous Nf1 +/- mouse line. The initial approach involved the phenotypic characterisation of this mouse model using a broad battery of rodent behavioural tests to examine specific aspects of cognition (including attention, working memory, short term memory, spatial memory, associative memory, cognitive flexibility), social function, and psychiatric traits (including anxiety and depression). We were able to replicate and expand previously published findings from the Nf1 +/- mouse model. Nf1 +/- mice showed altered spatial learning performance, object memory deficits and increased sociability. In addition, brains and striata of Nf1 +/- mice were significantly heavier relative to body weight when compared to controls. Intriguingly, several behavioural measures significantly correlated with gross brain anatomical measurements, providing supportive evidence for a mechanistic link between brain alterations due to Nf1 deficiency and the behavioural abnormalities observed. Future experiments will test promising new drug candidates in a preclinical study using Nf1 +/- mice, with the hope of rapidly progressing a successful candidate to clinical studies with NF1 patients. This research is funded by the Flicker of Hope Foundation.