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 nano-formulation exhibited enhanced free radical scavenging activity of 92% (IC50 value -29.27 +/- 2.6 mu g/ml), AChE inhibition of 95% (IC50 value -25.6292 +/- 1.5 mu g/ml) at its maximum dose (100 mu g/ml). CA@CaCO3 NFs attenuated the aggregation of beta-amyloid peptide (A beta) and also disaggregated the preformed mature plaques the major risk factor for AD. Overall, the present study reveals that CaCO3 nanoformulations exhibits potent neu-roprotective 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.

Automated summary

Alzheimer's disorder (AD) is a neurodegenerative disease with limited therapeutic options. In this study, a neuroprotective CaCO3 nanoformulation (CA@CaCO3 NFs) was developed by encapsulating the drug citronellyl acetate within CaCO3 nanoparticles. The CA@CaCO3 NFs showed enhanced antioxidant and AChE inhibitory activities, as well as the ability to attenuate and disaggregate beta-amyloid peptide (Aβ) plaques, a major risk factor for AD. Overall, this study suggests that CaCO3 nanoformulations have promising potential as a drug delivery system for the treatment of neurodegenerative and CNS-related disorders.