The identification of neuroprotectin D1 (NPD1), a biosynthetic product of docosahexaenoic acid (DHA), in brain and retina as well as the characterization of its bioactivity, is generating a renewed interest in the functional role and pathophysiological significance of omega-3 fatty acids in the central nervous system.Neurotrophins, particularly pigment epithelium-derived factor (PEDF), induce NPD1 synthesis and its polarized apical secretion, implying paracrine and autocrine bioactivity of this lipid mediator. Also, DHA and PEDF synergistically activate NPD1 synthesis and antiapoptotic protein expression and decreased proapoptotic Bcl-2 protein expression and caspase 3 activation during oxidative stress.In experimental stroke, endogenous NPD1 synthesis was found to be upregulated, and the infusion of the lipid mediator into the brain under these conditions revealed neuroprotective bioactivity of NPD1.The hippocampal CA1 region from Alzheimer's disease (AD) patients (rapidly sampled) shows a major reduction in NPD1.The interplay of DHA-derived neuroprotective signaling aims to counteract proinflammatory, celldamaging events triggered by multiple, converging cytokine and amyloid peptide factors, as in the case of AD. Generation of NPD1 from DHA thereby appears to redirect cellular fate toward successful preservation of retinal pigment epithelial (RPE)-photoreceptor cell integrity and brain cell aging. The Bcl-2 pro-and antiapoptotic proteins, neurotrophins, and NPD1, lie along a cell fateregulatory pathway whose component members are highly interactive, and have potential to function cooperatively in cell survival. Agents that stimulate NPD1 biosynthesis, NPD1 analogs, or dietary regimens may be useful as new preventive/therapeutic strategies for neurodegenerative diseases.

Aging is a complex biological process with many factors1. Regulation of a single ion such as phosphorus (Pi) can change with age. Pi takes part in cell signaling, energy metabolism and nucleic acid synthesis2. It is systemically regulated by the intestine and kidney3. Pi regulation declines with age3 and in diseases like diabetes mellitus and chronic renal disease. Disruption of Pi regulation can lead to disease in skeletal and cardiac systems, as well as further renal issues4. Since 85% of Pi is stored in the skeleton5, we focused on aging bone where the effects of systemic Pi dysfunction are apparent3. Mice aged 12, 80, and more than 100 weeks were euthanized. Femurs were harvested for gene expression analysis of Pi transporters, cytokines, and inflammatory markers. Fold‐changes in expression were determined using 2−ΔΔCτ method. The difference between age groups was analyzed using one way ANOVA. The results show that Pi homeostasis is not efficient with older age. Expression of Pi transporters and bone health markers both change with age. Understanding the link between chronic diseases and bone health is vital to the aging population for future management and prevention.