Exploring the Pathogenesis of Alzheimer's Disease and Revolutionary Treatment Strategy Based on Nanotechnology
Alzheimers disease (AD), a catastrophic disorder that commonly affects the elderly, causes extracellular plaques to form in the hippocampus, leading to slow, progressive loss of brain function. The Blood Brain Barrier poses a significant challenge for conventional drug delivery in AD therapeutics. Therefore, introducing novel strategies such as nanotechnology-based drug delivery offers promising potential. This paper highlights the significance of nanotechnology based drug delivery in AD with respect to its pathophysiology and discusses the current situation and future prospects of the same in diagnosis and therapy. Data collection involved scientific databases such as PubMed, Science Direct, and Google Scholar. The keywords searched were AD, neurodegenerative, nanotechnology, Amyloid-beta protein, tau protein and patents. A total of 146 papers were obtained. The pathophysiology of AD with respect to the Amyloid- and tau hypotheses were found to have significant therapeutic potential. It was also found that nanotechnology systems were able to offer enhanced site-specific action, offering a low toxicity profile in areas where conventional drug delivery systems had difficulty to act on. Delivery systems that were found to have potential were nanoparticles (NPs) including inorganic NPs and magnetic NPs, Quantum Dots, liposomes, dendrimers, Micelles, etc. Thus, our work suggests that NP-based drug delivery systems are able to overcome the challenges faced by conventional systems to achieve therapeutic efficacy with substantial levels of evidence, initiating the much-needed discussions on their potential use in AD therapeutics.
Publication Details
- Journal
- Journal of Biological Regulators and Homeostatic Agents/Journal of Biological Regulators & Homeostatic Agents
- Published
- 2024-08-30
- DOI
- https://doi.org/10.23812/j.biol.regul.homeost.agents.20243809.464
- Primary Topic
- Cancer Research and Treatment
- Type
- article
- Field-Weighted Citation Impact
- 0.00