Vedin, Inger, Cederholm, Tommy, Freund-Levi, Yvonne, Basun, Hans, Hjorth, Erik, Irving, Gerd Faxén, Eriksdotter-Jönhagen, Maria, Schultzberg, Marianne, Wahlund, Lars-Olof, Palmblad, Jan

Omega-3 fatty acids, e.g., dokosahexaenoic acid (DHA) and eikosapentaenoic acid (EPA), ameliorate inflammatory reactions by various mechanisms, but the role of prostaglandins remains unclear. Our aim was to determine if dietary supplementation with a DHA-rich fish oil influenced the release of PGF(2alpha) from peripheral blood mononuclear cells (PBMC). In the OmegAD study, 174 Alzheimer disease […]

Serrano-Pozo, Alberto, Vega, Gloria L., Lütjohann, Dieter, Locascio, Joseph J., Tennis, Marsha K., Deng, Amy, Atri, Alireza, Hyman, Bradley T., Irizarry, Michael C., Growdon, John H.

Preclinical and epidemiologic studies suggest a protective effect of statins on Alzheimer disease (AD). Experimental evidence indicates that some statins can cross the blood-brain barrier, alter brain cholesterol metabolism, and may ultimately decrease the production of amyloid-beta (Abeta) peptide. Despite these promising leads, clinical trials have yielded inconsistent results regarding the benefits of statin treatment […]

Squitieri, Ferdinando, Orobello, Sara, Cannella, Milena, Martino, Tiziana, Romanelli, Pantaleo, Giovacchini, Giampiero, Frati, Luigi, Mansi, Luigi, Ciarmiello, Andrea

Purpose: Huntington disease (HD) mutation increases gain-of-toxic functions contributing to glutamate-mediated excitotoxicity. Riluzole interferes with glutamatergic neurotransmission, thereby reducing excitotoxicity, enhancing neurite formation in damaged motoneurons and increasing serum concentrations of BDNF, a brain cortex neurotrophin protecting striatal neurons from degeneration.; Methods: We investigated metabolic and volumetric differences in distinct brain areas between 11 riluzole-treated […]

Steinacker, Petra, Klafki, Hans, Lehnert, Stefan, Jesse, Sarah, Arnim, Christine A. F. V., Tumani, Hayrettin, Pabst, Alice, Kretzschmar, Hans A., Wiltfang, Jens, Otto, Markus

The clinical diagnosis of Creutzfeldt-Jakob disease (CJD) can be supported by several biochemical markers in cerebrospinal fluid (CSF) such as 14-3-3 proteins and tau protein. Unfortunately, none of the currently known markers are suited for screening or seems to be directly related to the pathophysiological process. A marker fulfilling these criteria might facilitate the early […]