Solutions of C60, C60O, or C70 and metal complexes of octaethylporphyrin (OEPH2) yield crystals that contain both the fullerene and the porphyrin. The structures of C60·2CoII(OEP)·CHCl3, C60·2ZnII(OEP)·CHCl3, and C60O·2CoII(OEP)·CHCl3 are isomorphous and contain an ordered C60 cage surrounded by two MII(OEP) units. Although there is no covalent bond between the fullerene and porphyrin components, the separation between these units is shorter than normal van der Waals contact. Crystals of C70·CoII(OEP)·C6H6·CHCl3, C70·NiII(OEP)·C6H6·CHCl3, and C70·CuII(OEP)·C6H6·CHCl3 are also isomorphous with an ordered fullerene, but have only one porphyrin/fullerene contact. Crystalline C60·ClFeIII(OEP)·CHCl3 lacks the close face-to-face porphyrin/porphyrin contact that is common to all of the other structures reported here but retains the intimate contact between the porphyrin and the fullerene. In (C120O)·CoII(OEP)·0.6C6H6·0.4CHCl3 the fullerene dimer is enclosed by two CoII(OEP) moieties. Unfortunately disorder in the fullerene portion obscures details of the geometry of the bridging region between the fullerenes.

Environmental enrichment (EE) has been shown to improve cognitive performance and brain indices of cognition in normal mice and rats. Because the therapeutic potential of intensive, long-term EE to benefit patients with Alzheimer's disease (AD) has yet to be explored, the present study evaluated the effect of long-term EE on cognition in an animal model of AD, the APPsw transgenic mouse. Beginning at 16 months of age, APPsw mice were put into EE or standard housing for 4 months and then tested in four cognitive-based tasks (Morris maze, circular platform, platform recognition, and radial arm water maze) between 20 and 22 months of age. Our results indicate that long-term EE of aged APPsw mice results in global, overall improvement in cognitive function across these tasks without decreasing brain beta-amyloid (A beta) deposition. The results suggest that long-term EE/cognitive stimulation could provide cognitive stabilization or improvement to AD patients through mechanisms independent of A beta deposition and clearance.

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