Production and Evaluation of Lipid Nanoparticle as Drug Carrier for Treatment of Alzheimer’s Disease to Enhance the Blood Brain Barrier Penetration
S. Chitra, A. Sundar Raj, G. Yalini, K. Raghuram
2025
Abstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that most frequently affects older adults, resulting in cognitive impairment, memory loss, and behavioural changes. It is the most prevalent cause of dementia and an increasing global health issue with aging populations. The pathophysiology of AD is marked by amyloid-beta plaque deposition, tau protein tangle formation, and synaptic loss, leading to neuronal dysfunction and cell death. Despite the fact that existing pharmacological therapies may correct symptoms, they do not reverse or stop disease progression. One of the greatest obstacles to treating AD is the blood-brain barrier (BBB), which shields the brain from the effective delivery of therapeutic compounds and thus reduces the effectiveness of most drugs. This restriction necessitates novel drug delivery systems that have the ability to cross the BBB and deliver drug therapeutic agents in adequate concentrations into the brain. Lipid nanoparticles (LNPs) also present a potent solution to such a challenge. LNPs represent nanosized lipid-based carrier systems that encapsulate hydrophobic and hydrophilic drugs, providing an environment of a biocompatible platform for delivery of drugs as targeted therapy. The inherent characteristics of LNPs, including their nanoscale dimensions, flexibility, and capacity to alter surface chemistry, make them capable of interacting favourably with biological membranes and penetrating the BBB. This is a quality that makes LNPs especially ideal for delivering therapeutic agents to the brain. The therapeutic uses of LNPs in the treatment of AD are multifaceted, targeting the most important pathological characteristics of the disease, including amyloid-beta plaques and tau protein tangles. LNPs may be used to deliver small molecules, peptides, and antibodies to prevent amyloid-beta aggregation or facilitate clearance of amyloid-beta from the brain, perhaps delaying disease. RNA therapies such as siRNA and antisense oligonucleotides are deliverable through LNPs and can suppress production of amyloid-beta, serving as an alternate mechanism for modification of disease. Overall, lipid nanoparticles are a promising drug delivery system for Alzheimer's disease. Their capacity to penetrate the BBB, reach specific areas of the brain, and deliver therapeutic agents in controlled release makes them an important resource for treating the intricacies of AD.
DownloadPaper Citation
in Harvard Style
Chitra S., Raj A., Yalini G. and Raghuram K. (2025). Production and Evaluation of Lipid Nanoparticle as Drug Carrier for Treatment of Alzheimer’s Disease to Enhance the Blood Brain Barrier Penetration. In Proceedings of the 1st International Conference on Research and Development in Information, Communication, and Computing Technologies - ICRDICCT`25; ISBN 978-989-758-777-1, SciTePress, pages 168-181. DOI: 10.5220/0013924500004919
in Bibtex Style
@conference{icrdicct`2525,
author={S. Chitra and A. Raj and G. Yalini and K. Raghuram},
title={Production and Evaluation of Lipid Nanoparticle as Drug Carrier for Treatment of Alzheimer’s Disease to Enhance the Blood Brain Barrier Penetration},
booktitle={Proceedings of the 1st International Conference on Research and Development in Information, Communication, and Computing Technologies - ICRDICCT`25},
year={2025},
pages={168-181},
publisher={SciTePress},
organization={INSTICC},
doi={10.5220/0013924500004919},
isbn={978-989-758-777-1},
}
in EndNote Style
TY - CONF
JO - Proceedings of the 1st International Conference on Research and Development in Information, Communication, and Computing Technologies - ICRDICCT`25
TI - Production and Evaluation of Lipid Nanoparticle as Drug Carrier for Treatment of Alzheimer’s Disease to Enhance the Blood Brain Barrier Penetration
SN - 978-989-758-777-1
AU - Chitra S.
AU - Raj A.
AU - Yalini G.
AU - Raghuram K.
PY - 2025
SP - 168
EP - 181
DO - 10.5220/0013924500004919
PB - SciTePress