Regenerative marine waste towards CaCO3 nanoformulation for Alzheimer's therapy

Alzheimer's disorder (AD) is associated with behavioural and cognitive destruction with due respect to the neurological degeneration. Conventional therapeutic approach for treatment of AD using neuroprotective drugs suffered certain limitations such as poor solubility, insufficient bioavailability, adverse side effects at higher dose and ineffective permeability on blood brain barrier (BBB). Development of nanomaterial based drug delivery system helped to overcome these barriers. Hence the present work focused on encapsulating neuroprotective drug citronellyl acetate within CaCO3 nanoparticles to develop neuroprotective CaCO3 nanoformulation (CA@CaCO3 NFs). CaCO3 was derived from marine conch shell waste, while the neuroprotective drug citronellyl acetate was scrutinized by in-silico high throughput screening. In-vitro findings revealed that CA@CaCO3 nanoformulation exhibited enhanced free radical scavenging activity of 92% (IC50 value - 29.27 ± 2.6 μg/ml), AChE inhibition of 95% (IC50 value - 25.6292 ± 1.5 μg/ml) at its maximum dose (100 μg/ml). CA@CaCO3 NFs attenuated the aggregation of β-amyloid peptide (Aβ) and also disaggregated the preformed mature plaques the major risk factor for AD. Overall, the present study reveals that CaCO3 nanoformulations exhibits potent neuroprotective potential when compared to the CaCO3 nanoparticles alone and citronellyl acetate alone due to the sustained drug release and synergistic effect of CaCO3 nanoparticles and citronellyl acetate depicting the fact that CaCO3 can act as promising drug delivery system for treatment of neurodegenerative and CNS related disorders. [Display omitted] •CaCO3 nanoparticles was synthesized from marine waste shell of Chicoreus virgineus.•Neuroprotective agent Citronellyl acetate (CA) was selected by in-silico screening.•Nanoformulation (NFs) was fabricated by loading of CA with CaCO3 nanoparticles.•CA@CaCO3 NF showed antioxidant and AChE inhibitory activity.•Antiaggregation of Aβ peptide reveals CA@CaCO3 NF as potent neuroprotectant.