Sandra M. Cardoso

TL;DR: It is proposed that cellular demise and neurodegeneration in PD are due to the interplay between mitochondrial dysfunction, mitochondrial trafficking disruption, and impaired autophagic clearance.

TL;DR: This work studied the downstream signaling pathways induced by Aβ-mediated mitochondrial metabolism alterations and its consequences on cellular fate and shows for the first time that mitochondrial and cytosolic Aβ oligomers were significantly reduced upon microtubule dynamics re-establishment.

TL;DR: A set of natural‐based hybrid compounds by conjugation of a tacrine moiety with an S‐allylcysteine (garlic constituent) or S‐propargylcy Steine moiety aimed at improving the cholinergic system and neuroprotective capacity are explored.

TL;DR: It is demonstrated that mitochondrial preconditioning induced by cyanide triggers a protective response mediated by mitochondrial ROS and HIF-1α activation and signaling, which render brain endothelial and neuronal cells resistant against glucotoxicity.

TL;DR: The design and synthesis of the new hybrid compounds are described, followed by the assessment of solution properties, namely iron chelation and anti-oxidant capacity, and their effects on the viability of neuronal cells stressed with Aβ(42).