Therapeutic Potential of Rutin-Bound Glucose Carbon Dots for Alzheimer’s Disease / Sana Khan

By: Khan, SanaContributor(s): Supervisor : Dr. Aneeqa NoorMaterial type: TextTextIslamabad : SMME- NUST; 2023Description: 76p. Soft Copy 30cmSubject(s): MS Biomedical Sciences (BMS)DDC classification: 610 Online resources: Click here to access online Summary: World Health Organization (WHO) states that approximately 55 million people are suffering from dementia globally making it a major public health concern. Alzheimer’s Disease (AD) is the most common cause of dementia constituting 60-80% of cases worldwide. Currently, the available drugs can only provide symptomatic relief. The blood-brain barrier is one of the obstacles in the path of the drugs that limits them from reaching the target area in the brain. Carbon Dots (CDs) have excellent properties such as biocompatibility, low cytotoxicity, and large surface area to volume ratio which makes them a potential candidate for drug delivery. Rutin, a naturally occurring flavonoid has many biological effects, one of which is the neuroprotective effect. Previously, this drug has been found to reduce Aβ oligomer levels and neuroinflammation in APP/PS1 mouse model of AD with improvement in spatial memory. With the aim of improving its reach and effectiveness in the brain, in this study, nitrogen-doped carbon dots (NCDs) and Rutin were utilized to synthesize NCD-Rutin, which is a nanomaterial with high-performance capabilities. NCDs exhibited the ability to effectively suppress the hyperphosphorylation of tau protein. FTIR and UV-Vis Spectrum results confirm the doping of NCDs with Rutin. Additionally, utilizing AD-like rat model, it was observed that the NCD-Rutin was able to penetrate the bloodbrain barrier. Aluminum chloride injection (150 mg/kg/day) with D-galactose (300 mg/kg/day) was administered intraperitoneally for 15 days in order to induce AD-like condition in 1-year-old male albino rats. A single injection of NCD-Rutin (10 mg/kg) was administered intraperitoneally to experimental animals. Significant improvement in memory impairment was observed in ADlike rat models a week after the injection of NCD-Rutin, which demonstrates its potential as a promising therapeutic agent for AD treatment.
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World Health Organization (WHO) states that approximately 55 million people are suffering
from dementia globally making it a major public health concern. Alzheimer’s Disease (AD) is the
most common cause of dementia constituting 60-80% of cases worldwide. Currently, the available
drugs can only provide symptomatic relief. The blood-brain barrier is one of the obstacles in the
path of the drugs that limits them from reaching the target area in the brain. Carbon Dots (CDs)
have excellent properties such as biocompatibility, low cytotoxicity, and large surface area to
volume ratio which makes them a potential candidate for drug delivery. Rutin, a naturally
occurring flavonoid has many biological effects, one of which is the neuroprotective effect.
Previously, this drug has been found to reduce Aβ oligomer levels and neuroinflammation in
APP/PS1 mouse model of AD with improvement in spatial memory. With the aim of improving
its reach and effectiveness in the brain, in this study, nitrogen-doped carbon dots (NCDs) and Rutin
were utilized to synthesize NCD-Rutin, which is a nanomaterial with high-performance
capabilities. NCDs exhibited the ability to effectively suppress the hyperphosphorylation of tau
protein. FTIR and UV-Vis Spectrum results confirm the doping of NCDs with Rutin. Additionally,
utilizing AD-like rat model, it was observed that the NCD-Rutin was able to penetrate the bloodbrain barrier. Aluminum chloride injection (150 mg/kg/day) with D-galactose (300 mg/kg/day)
was administered intraperitoneally for 15 days in order to induce AD-like condition in 1-year-old
male albino rats. A single injection of NCD-Rutin (10 mg/kg) was administered intraperitoneally
to experimental animals. Significant improvement in memory impairment was observed in ADlike rat models a week after the injection of NCD-Rutin, which demonstrates its potential as a
promising therapeutic agent for AD treatment.

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