In the EU over 3 million people have Alzheimer’s disease (AD) and currently no therapies are available. Our research aim is to develop biocompatible multifunctional nanoparticles able to cross the blood-brain barrier reaching the brain, principal site of Alzheimer's disease, to target and destroy the amyloid deposits, characteristic of the illness. The results show that these nanoparticles (trade mark Amyposomes@) delay phenotype progression, prevent memory impairment and reduce amyloid plaques in mouse models of Alzheimer.


Gliomas, intrinsic brain tumours, are a dissimilar group of oncological diseases for which there is currently no cure. Among gliomas, glioblastoma multiforme (GBM, also called grade IV astrocytoma) is one of the most deadly brain tumors, with a short median patient survival and a very limited response to therapies. Our research aim is to specifically deliver chemotherapeutics to tumour cells, reducing their side effects, through smart bionanotech system. The results show that the product developed is able to reach the brain and to selectively trigger apoptosis in patient-derived xenografts (PDXs) rodent model.

THERAPY OF amyotrophic lateral sclerosis (SLA)

Despite more than 100 disease-modifying or neuroprotective agents have been tested in clinical trials, no cure for Amyotrophic Lateral Sclerosis (ALS) has yet been found. Our research aim is to validate targeted lipid-based particles as carrier for HK1-N-terminal based peptide (NHK1), which is able to restore the cell viability of motor neuron-like NSC-34 cells. The results show that these particles are able to deliver NHK1 peptide across the BBB, preserving its ability to counteract the oxidative stress in a ALS cellular model.


Different neurological disorders are strongly interwined with reactive oxygen species (ROS) production and oxidative stress, which are considered common effectors in the cascade of degenerative and pathological events in the brain. Our research aim is to test the antioxidant properties of Cerium oxide nanoparticles (CeONPs), thanks to theri ability known to act as strong, recyclable ROS scavengers by shuttling between Ce3+ (reduced) and Ce4+ (oxidized) oxidation states. The results show that CeONPs are able to strongly reduce the oxidative stress associated to beta-amyloid aggregates, typical hallmarks of Alzheimer's disease.