PRJNA719033
The moringin/a-CD complex attenuates neuronal death and promotes cellular repair in an in vitro model of Alzheimer's disease: a transcriptomic study.
Alzheimer s disease (AD) is a progressive neurodegenerative disorder and represents the most common form of senile dementia. In AD the hallmarks are the extracellular amyloid plaques, induced by amyloid beta (Abeta) and neurofibrillary tangles. Autophagy and mitophagy, are cellular processes that play a key role in the aggregation of beta-amyloid (Abeta), phosphorylation of tau, consequently, impairment of these processes lead to the progression of AD. Thus, interest is growing in the search for new natural compounds with neuroprotective, anti-amyloidogenic, antioxidative and anti-inflammatory properties that could usefully in the prevention of AD. Moringin (MOR), is an isothiocyanate that owns several biological activities, among which protective effects against neurodegenerative disorders. MOR conjugated with alpha-cyclodextrin (MOR/alpha-CD) forms a complex with improved solubility and stability in aqueous solutions. The aim of this work was to evaluate the efficacy of MOR/alpha-CD pre-treatment in an in vitro model of AD induced by exposure to Abeta 1-42 . We evaluated the transcriptional profile by next-generation sequencing (NGS). The pretreatment with MOR/alpha-CD reduced the expression of the genes which encode proteins involved in senescence, autophagy and mitophagy processes. Additionally, MOR/alpha-CD as able to induce neuronal remodeling, principally downregulating the Slit/Robo signaling pathway.