The establishment of effective molecular interventions to improve memory and alleviate memory deficits in disease remains a long-standing challenge despite growing molecular understanding of synaptic plasticity and memory formation. Capitalizing on the fact that long-term potentiation (LTP) requires N-methyl-D-aspartate receptors (NMDARs) and Ca/calmodulin-dependent protein kinase II alpha (CaMKIIα), we develop an intrabody that targets NMDARs and show that intrabody-mediated postsynaptic enrichment of CaMKIIα in the hippocampus improves contextual fear memory. This molecular approach suggests a potential demand for effective targeting of postsynaptic molecules to enhance memory and provides insights into studying memory improvement in health and disease.
View Article and Find Full Text PDFBackground: With the ageing population, lower urinary tract symptoms are becoming more prevalent with an estimate that by 2025, 52 million adults in the USA will be affected. After lifestyle modifications fail to resolve symptoms, second-line therapy with medications is often recommended by both the European Association of Urology and the American Urological Association. Considering the vulnerability of older patients to co-morbidities, physicians must be more aware of adverse side effects.
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