A defective blood-brain barrier (BBB) has been postulated to be present in Alzheimer's disease (AD), which would allow circulating beta-amyloid peptide to enter the brain. The authors tested this hypothesis by studying BBB function in 14 individuals with probable AD and 9 elderly control subjects. A computed tomographic method was used to measure blood-to-brain transport (K1), tissue-to-blood efflux (k2), tissue plasma space (Vp), and tissue extracellular space (Ve) of meglumine iothalamate. Repeated-measures analysis of variance indicated no significant differences between the groups for any of the measures. The authors conclude that there is no generalized abnormality of the blood-brain barrier in AD.

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These findings suggest that, using the single-needle anterior approach, the neurolytic spread in the celiac area is highly hampered by the regional anatomic alterations. It also appears that only a complete (four quadrants) neurolytic spread in the celiac area can guarantee long-lasting analgesia, and that this picture may be obtained in a very limited fraction of patients with regional anatomic alterations.

With indirect immunofluorescence, glutamate decarboxylase (GAD), the GABA synthesizing enzyme, was localized to cell bodies in the inner half of the inner nuclear layer and a few in the outer tier of the ganglion cell layer in the rhesus monkey retina. In the inner plexiform layer there were three strongly GAD-immunoreactive laminae separated by two less immunoreactive laminae. Electron microscopy demonstrated that the GAD was contained in amacrine cells and these GAD-immunoreactive amacrines were primarily pre- and postsynaptic to biopolar cell axon terminals. The GAD-containing processes possessed small synaptic vesicles and formed synapses that could be characterized as symmetrical. Large, dense-cored vesicles were often found in the cell bodies and synaptic processes of the GAD-immunoreactive amacrine cells. As the vast majority of the synaptic input and output of the GAD-containing amacrine cells was to and from bipolar cells and the strongest GAD-immunoreactivity correlated with the endings of bipolar cells that connect with a single cone, the functional effects of GABA in the primate retina are likely to be found in the responses of single cone pathways in the inner plexiform layer.