We have shown a possible effect of aging on tNAA and Glx levels, which should be taken into consideration when planning serial MRS imaging of the spinal cord in clinical and research settings. However, it will take further longitudinal studies to determine the rate of change in metabolites over time in healthy aging and whether metabolite concentrations decline at differing rates in spinal grey matter and white matter. Due to exploratory nature of the study, our sample size was relatively small and absolute metabolite concentrations observed within of our cohort should therefore be interpreted with some caution until future work, using larger sample sizes, further characterises absolute metabolite concentrations by age group. Future experiments should also allow additional scanning time for the inclusion of an experimentally measured macromolecular spectrum, as this has been shown to improve the accuracy of spectral quantification. Studies of brain aging have previously shown that age-related metabolite changes are not uniform and can vary between brain regions, and it is possible that metabolite changes during aging occur at dissimilar rates at different spinal levels which will also require further investigation. Pre-synaptic components, such as precursors of synaptic vesicles, active zone compartments, mitochondria and proteins essential for synaptic vesicle release must be transported down the axon to the nerve terminals by the anterograde motor kinesin-1. Upon arrival at the nerve terminal, cargo-loaded vesicles must undergo fusion with the plasma membrane to assemble active zones and reconstitute synaptic vesicles. Work has shown that bone morphogenetic protein growth factors regulate the development, growth and function of synapses in Drosophila via retrograde signaling. Interestingly, a mutation of the dynein–dynactin motor p150/glued disrupted retrograde axonal transport of activated BMP as assayed by the loss of its downstream signal phospho Mad accumulation in motor neuron nuclei, indicating that perhaps this signal could be incorporated into a signaling endosome that is transported by dynein motors, similar to the signaling endosome NGF-TrkA in neurotrophin signaling. However, whether such a BMP signaling endosome exists and whether this complex is transported via a direct interaction with molecular motors is unclear. Further, since the BMP ligands and receptors are expressed in multiple cells in the CNS how BMP signaling at the CNS plays a role in Dasatinib normal NMJ development and function at the distal ends of neurons is also unknown. In many neurodegenerative diseases problems in axonal transport and synapse function have been reported long before the onset of classical disease pathologies. However the mechanisms of how defects in axonal transport directly contribute to synaptic dysfunction is unknown. In Huntington’s disease mouse models, abnormal plasticity was seen before signs of disease or neuronal loss. Human studies revealed synaptic dysfunction decades before clinical diagnosis in HD carriers.