Several observations suggest a beneficial effect of melatonin antagonism for Parkinson's disease (PD). Although bright light therapy (BLT) suppresses melatonin release and is an established treatment for depression and sleep disturbances, it has not been evaluated in PD. We examined effects of BLT on motor symptoms, depression, and sleep in PD in a randomized placebo-controlled double-blind study in 36 PD patients, using Parkinson's Disease Rating Scale (UPDRS) I-IV, Beck's Depression Inventory, and Epworth Sleepiness Scale. All patients received BLT for 15 days in the morning, 30 min daily. Illuminance was 7.500 lux in the active treatment group and 950 lux in the placebo group. Although group differences were small, BLT led to significant improvement of tremor, UPDRS I, II, and IV, and depression in the active treatment group but not in the placebo group. It was very well tolerated. Follow up studies in more advanced patient populations employing longer treatment durations are warranted.

The interaction of the sulfatide activator protein with different glycosphingolipids has been studied in detail. The following findings were made.1. 2. In the absence of degrading enzymes the activator protein acts in vitro as a glycosphingolipid transfer protein,transporting glycosphingolipids from donor to acceptor liposomes. Lipids having less than three hexoses, e.g. galactosylceramide, sulfatide and ganglioside GM3 were transferred at very slow rates, whereas complex lipids such as gangliosides GMZ, GMl and GDla were transferred much faster than the former. The transfer rate increased with increasing length of the carbohydrate chain of the lipid molecules.3. Both the acyl residue in the ceramide moiety and the nature of the carbohydrate chain are significant for recognition of the glycosphingolipids by the sulfatide activator protein. Apparently, both residues serve as an anchor and the longer they are the better they are recognized by the protein.4. In the absence of activator protein, degradation rates of sulfatide derivatives by arylsulfatase A, and of ganglioside GM1 derivatives by P-galactosidase, increase with decreasing length of acyl residues in their hydrophobic ceramide moiety. Addition of activator protein stimulates the degradation of only those GM1 and sulfatide derivatives that have long-chain fatty acids in their hydrophobic ceramide anchor.Glycosphingolipids are components of the outer leaflet of plasma membranes. They form cell-type-specific patterns on the surfaces of mammalian cells. These patterns change characteristically with differentiation and oncogenic transformation [l].Correspondence to K. Sandhoff, Institut fur Organische Chemie und Biochemie der Universitat Bonn, Gerhard-Domagk-Strasse 1, W-5300 Bonn 1, Federal Republic of Germany Abbreviations. Cer, ceramide or N-acylsphingoid; Sph, D-erythrosphingosine; NeuAc, N-acetylneuraminic acid; GalNAc, 2-acetamido-2-deoxy-~-galactose; GalCer, galactosylceramide; GlcCer, glucosylceramide; LacCer, lactosylceramide; sulfatide or 3'-O-sulfogalactosyl-ceramide; globotriaosylceramide or GbOse3Cer or Galcll + 4Galpl --f 4Glc/l1+ 1Cer; lysosulfatide or 3'-O-SUlfO-galaCtOSy1-Derythro-sphingosine; C,-sulfatide, derivative of sulfatide containing acyl chains with x C atoms (x = 2, 6, 18); G M~, I13NeuAc-LacCer or Gal(3+2clNeuAc)~l+4Glc~I +lCer; G M Z ,

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