Curcumin-Like Compounds as Neuroprotective Agents: Interactions with HSP60 and Amyloid Beta Peptide

Alzheimer’s Disease (AD) represents a fundamental challenge for public health in the 21st century. Current ADtherapies largely focus on symptomatic aspects of the clinical pathology, but they have yet to demonstrate anymajor impact on the disease progression [1]. The most important role of the research aimed at fighting the AD isthe development of neuro-protective agents, able to interfere with the protein aggregation process whose clinicalsignature is represented by the plaques deposition. An important role in AD’s framework could be played byHeat shock proteins (HSPs), highly regulated proteins that mediate the proteins proper folding and promoterecovery of their native conformations lost due to stress [2]. Recently, it was shown that HSP60 mediatestranslocation of Amyloid Precursor Protein (APP) and Amyloid Beta peptide (Aβ) to the mitochondria, leadingto dysfunction of the organelle [3]. In the field of potential therapeutic approaches, curcumin, a non-toxiccomponent of the curry spice turmeric, with anti-inflammatory, antioxidant and anti-aggregation properties, isemerging as a lead-compound for the development of neuro-protective drugs [4]. Here we present our recentfindings on Curcumin and Curcumin-like drugs obtained by a combination of cellular and in-vitro experiments,such as Thioflavine T fluorescence spectroscopy and Small Angle X-ray Scattering [5]. In particular, togetherwith the synthesis of some curcumin-like compounds, we present the results about their effect on a neuronal cellmodel, concerning the cytotoxicity and ability to affect Hsp60 expression, as well as their influence on Aβaggregation, provided by in vitro experiments.