Influence of sialic acid on the surface hydrophobicity of membranes

5-HIAA in the caudate nucleus (Alzheimer, 3.2 f 1.7; control, 5.2k2.3; P< 0.01), HVA in the caudate nucleus (Alzheimer, 13.5k5.0; control, 24.6k7.3; P<O.OI) and HVA in putamen (Alzheimer, 2.3 k0.9; control, 4.7k2.6; P<0.002). The highest CSF concentration of HVA is in the lateral ventricles, which are adjacent to the dopamine-rich caudate nucleus. Therefore, it seems likely that the CSF deficit of this metabolite in Alzheimer's disease reflects loss of HVA from this structure. 5-HIAA is not enriched in the caudate nucleus so a major influence of other brain regions may occur (e.g. the metabolite concentration is reduced in Alzheimer cortex; Bowen et al., 1979; Cross et al., 1983). Do the present deficits of amine metabolites reflect loss of parent neurotransmitters? Reduced amounts of serotonin (nmol/entire region) were found in both the caudate nucleus (Alzheimer, 0.8fO.3; control, 1.6fO.7; P<O.OI) and putamen (Alzheimer, 1.1 k0.7; control, 3.2f 1.0; P< 0.001), whereas no significant alterations in dopamine content occurred in either the caudate nucleus (Alzheimer, 13.2f 10.4; control, 16.4f4.2) or putamen (Alzheimer, 24.3 f 14.9; control, 36.8 k 10.6). This contrasts with the changes seen in Parkinson's disease (Marsden, 1982), where severe neostriatal deficits in both dopamine and HVA reflect loss of nigrestriatal neurons. The present findings, therefore, suggest sparing of nigrestriatal neurons in Alzheimer's disease, together with loss of raphe-striatal serotonergic neurons, consistent with neurohistological data (Ishii, 1966; Mann & Yates, 1983).