Traumatic brain injury (TBI) is one of the leading causes for death or disability involving an initial mechanical damage that leads to the destruction of the brain matter and adjacent vasculature, producing a lesion cavity. The treatment options are limited to stabilizing the patients and treating secondary symptoms. Those secondary injuries appear in a time-shifted manner and include axonal injury leading to neuronal death, a process not fully understood yet. For several central nervous system (CNS) injury models including spinal cord injury, it was already shown that the growth factor-activated phosphatase and tensin homolog (PTEN)/protein kinase B (AKT) pathway is involved in axonal regeneration. We hypothesize that the pharmacological modulation of the PTEN/AKT-pathway improves regeneration after TBI – a connection that has not been investigated so far in great detail. Thus, different compounds have been tested in vitro – a PI3K activator (1938), an AKT activator (SC79) and three different PTEN inhibitors (bpV HOpic, bpV phen, SF1670). A first visual inspection suggests that the neurite length could be affected by the different compounds, which will be further investigated with the image processing tool AutoNeuriteJ for a morphometric analysis. In addition, the compounds were tested with growth-inhibiting conditions to evoke a potential effect that may be masked in growth-supporting conditions. If the neurite growth analysis in primary cell culture proves a significant effect of different compounds on neuronal growth, the compounds will be tested in an in vivo model of TBI using a rodent weight-drop model.