Neuroprotective Effect Of Cymbopogon nardus And Polygonum glabrum On Alcohol-Induced Alzheimer In Rats


  • Pankaj Singh Research scholar, Sunrise University, Alwar Rajasthan.
  • Jitendra Malviya Research supervisor, Sunrise University, Alwar Rajasthan.


Alzheimer, oxidative stress, ethanol


Alzheimer's disease (AD) is a degenerative neurological condition that gradually worsens over time. It is marked by a decline in cognitive function, including memory loss, and changes in behaviour. AD aetiology is influenced by several variables, including genetics, environment, and lifestyle. Alcohol use is a risk factor that may be changed and has the potential to impact the structure and function of the brain. Prolonged alcohol use may cause neuroinflammation, oxidative stress, and neuronal death, resulting in cognitive impairment and dementia. Nevertheless, the impact of alcohol on the developing brain remains little understood. This research examined the effects of alcohol on the brains of adult rats and explored the possible therapeutic benefits of extracts from Cymbopogon nardus L. and Polygonum glabrum L. for treating Alzheimer's disease. We used a rat model to simulate the drinking behaviour of human adolescents, namely binge ethanol consumption. The rats were subjected to subcutaneous administration of ethanol at a dosage of 2 g/kg every day for a duration of 21 days. Subsequently, rats who had received treatment were exposed to behavioural and biochemical assessments. Our investigation revealed that excessive ethanol consumption has a detrimental effect on the ability of adult rats to acquire and remember spatial information, as shown by the Morris water maze tests. Ethanol furthermore decreased the number of dendritic spines and synaptic proteins in both the hippocampus and cortex, which suggests the occurrence of synaptic injury. In addition, ethanol elevated the concentrations of pro-inflammatory cytokines, oxidative stress indicators, and apoptotic proteins in the brain regions. The administration of extracts effectively corrected the cognitive impairments, loss of synaptic connections, inflammation of brain tissue, oxidative damage, and death of neurones caused by ethanol exposure. The findings of our study indicate that exposing teenage rats to binge alcohol leads to persistent neurodegeneration and cognitive impairment in adulthood. However, these negative effects may be mitigated by the administration of BMCT, AMCT, WCO, and HAEPG. This work offers novel perspectives on the processes behind alcohol-induced brain damage and the potential advantages of using extracts as a therapy to prevent or manage alcohol-related dementia.Utilising any metric to evaluate dementia clinically, whether in individuals with cognitive impairments or in the general population, is inherently constrained. Having a thorough understanding of these limitations allows us to make informed decisions in selecting appropriate scientific methods to customise our neuropsychological assessment or consider alternate measures.

In the end, there could be a middle ground due to these constraints; yet, scientific knowledge has provided us with a more comprehensive understanding of the progression of dementia than ever before. By using advanced technologies like MRI, fMRI, PET, and SPET scans, together with cognitive testing conducted at certain intervals, including follow-ups, clinicians now have a greater ability to provide a more accurate diagnosis and prognosis compared to previous methods. It is expected that this would help educate service providers in expanding access to individuals with learning difficulties who also have dementia.

Keywords: Alzheimer, oxidative stress, ethanol