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Among cerebral functions, memory seems to be extremely sensitive to the aging process, particularly in the pathological condition. In this case memory decline is one of the first and more consistent symptoms observed.The similarities between the memory deficit induced by anticholinergic drugs and by elderly people have been the origin of the cholinergic hypothesis of geriatric memory.' Cholinomimetics and/or acetylcholine precursors have been tentatively used in geriatric patients to facilitate and improve memory function. Unfortunately the results obtained with this therapeutical approach have not been consistent. We now report the pharmacological effect of a natural compound, phosphatidylserine, on the v) L m .. L 3 n * 0 30 CONTROL ec-ps FIGURE 1. Effect of chronic treatment of BC-PS on EEG abnormalities in middle-aged rats.Rat chronically implanted with EEG electrodes were recorded for 30 minutes after 10 minutes of adaptation. EEG analyses were performed by computer. 504

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In the present study the topology and the biochemical mechanisms underlying the functional recovery of the dopaminergic nigrostriatal system is further analyzed. Rats with unilateral hemitransection were treated with 30 mg/kg GM1 monosialoganglioside or with its internal ester derivative for different periods of time. GM1 enhances 3H-dopamine uptake in striatal synaptosomes of the lesioned side, and the enhancement of dopamine uptake precedes that of striatal tyrosine hydroxylase activity. The above biochemical effects are accompanied by changes in behavioral- and electrophysiological-related parameters. The effect of GM1 on striatal tyrosine hydroxylase of the lesioned side disappears when the ascending dopaminergic fibers are extensively lesioned. This suggests that the source of regrowing dopaminergic nerve terminals in the striatum of partially lesioned rats resides mainly in the intact axons remaining in the ipsilateral side. When GM1 is injected into partially lesioned rats kept in darkness, no effect on tyrosine hydroxylase activity is observed. This indicates that the mechanism through which GM1 acts involves a normal light-dark cycle.

The present study deals with the developmental profile of cytosolic and membrane-bound gangliosides in rabbit whole brain from the 21st day of pregnancy, the time at which brain could be macroscopically recognized and handled, till birth. In this period of prenatal life the content of membrane-bound gangliosides showed a 2.5-fold increase, referred to fresh and dry brain weight and to membrane-bound protein; the content of cytosolic gangliosides reached a maximum at 21-22 days of pregnancy, and then underwent to birth a threefold diminution. The qualitative pattern of membrane-bound gangliosides, in the same period of life, was characterized by an increase of GD1a and GM1 (more marked for GD1a), a decrease of GT1a, GT1b and GQ1b, and a constant level of GD3 and GD1b. At 21 days of pregnancy the most abundant gangliosides were GT1b and GQ1b, followed by GD1a and GD1b; at birth it was GD1a, followed by GT1b, GD1b and GM1. The qualitative pattern of cytosolic gangliosides closely resembled, during the entire period of prenatal life examined, that of membrane-bound gangliosides.