PUBLICATION
Chrysin-Loaded Chitosan Nanoparticle-Mediated Neuroprotection in Aβ1-42-Induced Neurodegenerative Conditions in Zebrafish
- Authors
- Saleem, S., Banerjee, R., Rajesh Kannan, R.
- ID
- ZDB-PUB-220614-15
- Date
- 2022
- Source
- ACS Chemical Neuroscience 13(13): 2017-2034 (Journal)
- Registered Authors
- Keywords
- Alzheimer’s disease, behavior, brain, memory, nanotechnology, neurodegeneration
- MeSH Terms
-
- Alzheimer Disease*/drug therapy
- Amyloid beta-Peptides/therapeutic use
- Amyloid beta-Peptides/toxicity
- Animals
- Chitosan*/pharmacology
- Chitosan*/therapeutic use
- Flavonoids
- Nanoparticles*
- Neurodegenerative Diseases*
- Neuroprotection
- Peptide Fragments
- Plaque, Amyloid
- Zebrafish
- PubMed
- 35696319 Full text @ ACS Chem. Neurosci.
Citation
Saleem, S., Banerjee, R., Rajesh Kannan, R. (2022) Chrysin-Loaded Chitosan Nanoparticle-Mediated Neuroprotection in Aβ1-42-Induced Neurodegenerative Conditions in Zebrafish. ACS Chemical Neuroscience. 13(13):2017-2034.
Abstract
Amyloid β plaques and neurofibrillary tangles are the characteristic features of Alzheimer's disease (AD). Plaques of amyloid β play a pivotal role in affecting cognitive functions and memory. Alzheimer's disease is a progressive neurodegenerative disease and is one of the leading causes of dementia worldwide. Several treatment strategies focusing on the amyloid cascade have been implemented to treat AD. The blood-brain barrier (BBB) poses the main obstructive barrier by refraining drugs from penetrating the brain. Nanotechnology is a promising research field for brain drug delivery using nanosized particles. Zebrafish is emerging as a model of interest to elaborate on brain targeting and nanotechnology-based therapeutics for neurodegenerative diseases. In the current study, we have synthesized and characterized chrysin-loaded chitosan nanoparticles (Chr-Chi NPs) and evaluated them for neuroprotection against amyloid-β-induced toxicity. We find that treatment with Chr-Chi NPs helps to retain memory, cognition, and synaptic connections, which are otherwise compromised due to Aβ1-42 toxicity. The NPs further help in reducing aggregates of amyloid β, thus decreasing neuronal death and generation of reactive oxygen species (ROS). Taken together, our study brings to light a novel strategy for treating AD by a combined action on the neurons and amyloid aggregates mediated by chrysin and chitosan, respectively. Chr-Chi NPs, therefore, have the potential to provide a beneficial combinatorial treatment strategy for AD.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping