Neuropsin is associated with MAP2c dependent dendritic morphology in aging brain

Brain aging associated impairment in synaptic plasticity and memory increases vulnerability for neurodegenerative pathologies. However, lacunae in understanding the molecular mechanisms underlying such impairment have hindered the development of recovery strategies. In this context, the emerging evidences for modifying the synaptic morphology by activity dependent plasticity proteases are noteworthy. Neuropsin (NP) is one such serine protease implicated in synaptic plasticity and memory acquisition, though it has never been explored in aging brain. Recently, we reported regional variation of NP expression in aging mouse brain. It was predominant in forebrain regions exhibiting age dependent decline in cerebral cortex, sharp increase in adult olfactory bulb and hippocampus and thereafter reduction in old age. The expression pattern of NP was strongly correlated with cleavage of its substrate, L1CAM and downstream dendritic marker MAP2c level in different brain regions during aging. In the present research highlight, we provide a brief overview of our laboratory findings related to brain aging with particular focus on NP expression and its implication in MAP2c dependent dendritic morphological changes. Such novel findings suggest NP as a potential therapeutic target for age associated decline in memory and related disorders.