Abstract: The present invention relates to compositions comprising spermidine and/or a pharmaceutically acceptable salt thereof for use in the prevention and/or alleviation of side effects caused by nicotinamide, nicotinic acid and/or a pharmaceutically acceptable salt thereof.

Abstract: The present invention relates to methods and means for inhibiting or preventing the growth of fungal cells with at least one flavone selected from the group consisting of 5-methoxyflavone, 2?-methoxyflavone, 7-methoxyflavone, 3?,4?,5,7- tetrametoxyflavone, 3?,4?,5?,5,6,7-hexymethoxyflavone, 7,8-benzoflavone and 5,6-benzoflavone for inhibiting or preventing the growth of a fungal cell, wherein said flavone is used in combination with at least one further antimycotic compound selected from the group of azoles, both in an amount to exhibit a synergistic effect compared to the separate use of said flavone and said antimycotic compound.

Abstract: The present invention relates to methods and means for inhibiting or preventing the growth of non-filamentous biofilm forming fungal cells with at least one flavone of formula (I) wherein R1, R2, R3, R4, R5, R6 and R7 are independently from each other H or OH.

Abstract: Disclosed is a method for enhancing mitochondrial respiratory activity in a subject in need thereof that includes administering spermidine or a spermidine comprising extract to a subject in need thereof. The method includes the treatment and/or amelioration of mitochondrial energy disorders or diseases. The spermidine or a spermidine comprising extract can be extracted from plants or parts thereof, such as from legumes or grains or germs of legumes or grains, particularly from soya or wheat germs.

Abstract: The present invention relates to spermidine or spermidine comprising extracts for use in the treatment and/or amelioration of mitochondrial energy disorders or diseases.

Abstract: It is demonstrated that alpha synculein toxicity such as ?-synuclein mediated cell death, and alpha synuclein induced reactive oxygen species (ROS) in a cell requires proapoptotic endonuclease G and that the deletion of the endonuclease G or suppressing of the endonuclease G apoptotic pathway attenuates or counteracts such alpha synuclein toxicity. In view of these observations, compositions and methods for inhibition of ?-synuclein toxicity are provided. The inhibiting ?-synuclein toxicity can be used in methods for the treatment of synucleinopathies, such as Parkinsons disease (PD), dementia with Lewy bodies (DLB), pure autonomic failure (PAF), and multiple system atroypy (MSA) and the manufacture of medicaments for such treatment.

Abstract: The present invention relates to a method of treating a life threatening condition in a critically ill human patient with a non-infectuous disorder, wherein the critically ill patient is a patient receiving enteral or parenteral nutrition, the method comprising the step of administering to said patient an autophagy inducing agent.

Abstract: Present inventions demonstrates that alpha synuclein toxicity such as ?-synuclein mediated cell death, alpha synuclein induced reactive oxygen species (ROS) in a cell requires the proapoptotic endonuclease G and that the deletion of the endonuclease G or suppressing of the endonuclease G apoptotic pathway attenuates or counteracts such alpha synuclein toxicity. The present invention compositions and methods for inhibition of ?-synuclein toxicity. The inhibiting ?-synuclein toxicity can be used in methods of treatment of synucleinopathies, such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), pure autonomic failure (PAF), and multiple system atrophy (MSA) and the manufacture of medicaments for such treatment.