Cell Death Pathways in Mutant Rhodopsin Rat Models Identifies Genotype-Specific Targets Controlling Retinal Degeneration.

Retinitis pigmentosa (RP) is a group of inherited neurological disorders characterized by rod photoreceptor cell death, followed by secondary cone cell death leading to progressive blindness. Currently, there are no viable treatment options for RP. Due to incomplete knowledge of the molecular signaling pathways associated with RP pathogenesis, designing therapeutic strategies remains a challenge.

Potential Synergies of -Hydroxybutyrate and Butyrate on the Modulation of Metabolism, Inflammation, Cognition, and General Health.

The low-carbohydrate high-fat diet (LCHFD), also known as the ketogenic diet, has cycled in and out of popularity for decades as a therapeutic program to treat metabolic syndrome, weight mismanagement, and drug-resistant disorders as complex as epilepsy, cancer, dementia, and depression. Despite the benefits of this diet, health care professionals still question its safety due to the elevated serum ketones it induces and the limited dietary fiber. To compound the controversy, patient compliance with the program is poor due to the restrictive nature of the diet and symptoms related to energy deficit and gastrointestinal adversity during the introductory and energy substrate transition phase of the diet.

Anti-ageing glycoprotein promotes long-term survival of transplanted neurosensory precursor cells.

Cell therapy, to replace lost tissue, is a promising approach for the treatment of various neurodegenerative diseases. Many studies suggest, however, that the percentage of transplanted cells that survive and undergo functional integration remains low as a result of immune rejection, suboptimal precursor cell type, trauma during cell transplantation, toxic compounds released by dying tissues or nutritional deficiencies. We recently developed an ex vivo system to facilitate identification of factors contributing to the death of transplanted neuronal (photoreceptor) cells and compounds that block these toxic effects.