'TrkB expression at the neuromuscular junction is reduced during aging [Personius et al., Muscle and Nerve 2013]- Article Review Tyrosine Kinase B (TrkB) acts as a receptor for BDNF and NT- 4/5, which relates to the canonical nerve growth factor and the survival of motor and sensory neurons, respectively. This report assessed the hypothesis that the reduction of TrkB expression at the neuromuscular junction (NMJ) impacts acetylcholine receptors (AChRs). The investigation compared the function of full- length TrkB (trkB.FL) and truncated TrkB (trkb.t1) colocalized with AchRs at the NMJ across age groups. It was concluded that reduced expression demonstrates age-associated alternations, involving synaptic instability due to fragmentation of postsynaptic AChRs, alongside neurotransmission failure and muscle function. On average, 12- and 24-month-old mice had atrophied muscle fibres with compressed AChR regions, as shown by reduced TrkB immunolabelling, supporting the hypothesis. This alludes to the idea that TrkB-mediated signalling may be a neurotrophic signal for NMJ stability and growth. Therefore, the maintenance of sufficient TrkB signalling is potential therapeutic aid to improve muscle function during aging. TrkB expression was reduced in the slow- twitch soleus of 3-, 12- and 24-month-old male C57BL/6J mice. The scientific procedures carried out aimed to measure: AChR area, perimeter, TrkB immunolabel area and AChR-TrkB overlap. The muscles of each age group were prepared for immunolabelling; muscles were incubated with primary then secondary antibodies to label extracellular portions, presynaptic vesicles and neurofilaments of both TrkB.FL and TrkB. t1. The use of bright nerve labelling showed that the anti-TrkB antibody had access to the NMJ and provides visual aid to compare how neuronal activity in other results differs to the control. TrkB expression was quantified by the percentage colocalization between TrkB receptors with AChRs as they are postsynaptically co-expressed at the NMJ. The extent of colocalization was analysed using Image J, a valuable tool that allows the stacking of different images to allow easier comparison between them. Using cloned TrkB.FL PCR products, a calibration curve was constructed to assess mRNA levels in samples, allowing quantitative analysis of mRNA expression across age groups compared to TrkB expression. This report gave clear and extensive evidence that supports the hypothesis that TrkB signalling is reduced during senescence. Many experimental techniques, such as bright nerve labelling, allowed the researchers to compare results to various controls which helped ensure validity of results. However, the research was limited by the relatively small sample size (17 mice); future studies could involve a larger sample size to allow more valid results, with the impact of outliers being greatly reduced. Additionally, images that did not have exceptional neuronal labelling were disregarded when quantifying the expression of TrkB, which may have reduced the overall accuracy of the findings as well as reliability, as results that may have negatively impacted the general trend were excluded.