Essay On Resveratrol

We’ve known for a long time that red wine and dark chocolate can prevent sadness and boredom. Researchers a few years back suggested that the antioxidant resveratrol present in both treats might have heart benefits, although the significance of those claims is still being interrogated. Now, scientists are examining the possibility that resveratrol might work to prevent the onset of Alzheimer’s or slow its progression in existing cases.

The purpose of the experiment was to understand and determine the influence of Traumatic Brain Injury (TBI) on the spinal cord, and how the dietary Omega-3 (n-3) a fatty acid could counteract these effects. Not much is known about the effects of TBI on motor centers in the spinal cord. We are now starting to understand that TBI reduces the expression of some molecules that are critical for synaptic plasticity of the spinal cord.

The amyloid precursor protein (APP) is long associated with Alzheimer’s disease (AD). It is a single-pass transmembrane protein and is responsible for producing the neurotoxic Aβ plaque which accumulates within the brain (O’Brien et al. 2011). This accumulation of Aβ is what characterises AD. However, in spite of APP’s detrimental role in the pathogenesis of AD, it has been recently shown that APP can act as a neuroprotective molecule following traumatic brain injury (TBI). Approximately 10 million people worldwide are affected by this disease every year and it is projected that by 2020, TBI will surpass various diseases and become a major disease of burden (Hyder et al. 2007). Thus, due to this increase in morbidity and burden, TBI is an urgent medical and public problem.

CsA as a Neuroprotective Agent: Benefits and Caveats. A number of experimental studies have demonstrated that CsA exhibits significant cytoprotective properties in traumatic brain injury (TBI), cerebral ischemia, and reperfusion injury following acute myocardial infarction. Given these observations, phase I clinical trials have been performed and follow-up trials are currently proposed to examine CsA as a therapy for the treatment of acute TBI (Empey et al. 2006). In addition, a recently published clinical study reported compelling evidence that CsA administration at the time of reperfusion results in a smaller infarct size in patients undergoing percutaneous coronary intervention (Piot et al. 2008). However, a role for CsA as a neuroprotective agent in experimental models of acute SCI is inconclusive as several studies report beneficial effects while others conclude that CsA is ineffective

Pramipexole (PX) is a dopamine receptor agonist which has proved for its neuroprotective activity against cerebral ischemia. It shows its neuroprotective activity by having antioxidant [6], hypothermic and D3 receptor agonistic property in ischemic brain injury [7]. Hypothermia is the most promising neuroprotective strategy so far due to its lowering metabolic demand, reduction in calcium influx, suppression of inflammatory response and reduction in reactive oxygen species (ROS) generation [8]. Ischemic stroke produces excessive amount of ROS [9]. A drug like N-acetylcysteine (NAC) is well known for its quenching effect on ROS thereby it prevents cellular damage. Previous literature proved that NAC is neuroprotective for the reason that it has antioxidant property and neurovascular protective effects

Ischemic brain stroke represents the most common cause of serious morbidity and the second most common cause of mortality worldwide. Along with that traumatic brain injury also contributes a significant number of mortality and morbidity. While spontaneous recovery of lost functions to a certain degree takes place in some patients, the majority never regain full functional independence and ultimately suffer from a reduced quality of life. Clearly these health burden seeks detailed exploration of clinical and pathological aspects to modify the present treatment strategies. Glial scar formation which constitutes reactive astrocytes, microglia, endothelial cells, fibroblasts and extracellular components is the response of CNS after external assault.

The Role of Angioneurins in Neurodegeneration, adapted from the original table by Zacchigna et al, 2008 (28)

Importantly synaptic dysfunction occurs early in AD, while actual loss of synapses does not appear until much later in the disease. The loss of synaptic density leads to inhibition of the excitatory transmission in both the hippocampus and cerebral cortex, leading to significant memory loss [54, 55]. Although Aβ deposition and tau phosphorylation may induce neuronal loss, the predominant mechanism accounting for-synaptic thinning is more likely progressive neuronal apoptosis. Several factors have been shown to stimulate apoptosis in various models of AD, including, impaired glucose metabolism, excitotoxicity and mitochondrial dysfunction. Additionally, factors, such as tumor suppressor protein p53, forkhead box protein (FOXO), and ROS, can mediate apoptosis in AD [56, 57]. Thus, new treatment strategies aimed at developing molecules that downregulate apoptosis are currently a primary

Neuroprotection is a term used to refer to strategies and relative mechanisms that shield the central nervous system (CNS) from neuronal injuries caused by chronic (e.g., Alzheimer’s and Parkinson’s diseases) or acute (e.g., stroke) neurodegenerative diseases (NDs) [1]. These acute or chronic diseases result from breakdown and deterioration of neurons of the CNS and often result to the deterioration of the cognitive as well as the intellectual faculties of the sufferers. The onset of NDs symptoms are usually gradual as well as progressive, and includes loss of memory, primarily short-term, difficulty in learning, motor coordination, and many other functional loses [2, 3].

GSH is playing an important role in protecting some brain cells from reactive oxygen species which mean that the deficient in G6PD could be a risk factor for some neurodegenerative diseases. On the other hand, in different brain region and different cell types the oxidative damage of these area could have associated with pathological factors such as increasing the neuronal nuclear diameter, increased vaculation and increased prevalence of chromatolytic neurons which could happen after losing Purkinje cells

Critical events in ischemic cascade. Adapted from Midori et al. (2012) (17). Following ischaemia, the deprivation of oxygen and glucose to the brain lead to loss of ATP (energy loss) and ion pump failure. The loss of ion concentration gradients causing to cytotoxic oedema and releasing of excitatory amino acids (EAAs). Following glucose lessening cell aerobic metabolism switch to anaerobic, which resulting to metabolic acidosis. All of these events lead to cell death, or necrosis. Ischaemia also caused to the upregulation and activation of many immediate early genes and stress signals, which lead to inflammatory responses, cell apoptosis and, subsequently, activation of matrix metalloproteinases (MMPs) as a damaging protease which can lead

Meanwhile, rats that were given riluzole an hour to four hours after injury have reduced neuronal loss. It also prolonged the rats’ lives after injury as compared to those who received different

Resveratrol, 3,4’,5-trihydroxystilbene (MW: 228.2) is a naturally occurring polyphenol and phytoalexin with a stilbene structure (Carrizzo et al., 2013). There are various sources of resveratrol such as grapes, peanuts and mulberries. In 1940, it was first detected in the roots of white hellebore (Veratrum grandiflorum) and in 1963, it was isolated from the roots of traditional Chinese medicinal plant, Polygonum cupsidatum (Langcake et al., 1977;Vaz-da-Silva et al., 2008). The basic structure of resveratrol comprises of two phenolic rings linked by a double styrene bond, which is responsible for the cis and trans isomeric forms (Gambini et al., 2015). Exposure to ultraviolet light converts the biologically active trans-resveratrol to inactive

Brain is highly susceptible to complicated consequences of blood flow reductions leading to its altered function which is termed as ischaemia. Focal ischaemia and global ischaemia are the main forms of stroke. Middle cerebral artery occlusion is the main cause of focal ischaemia. Cardiac arrests, shock which creates hypoxia, hypoglycemia of increased metabolic rate of brain cells lowered cerebral perfusion pressure are the causes for global ischaemia. Focal ischemia leads to irreversible cellular damage in brain. Specific thresholds of ischaemia for particular areas in brain are figured. White matter region of the brain is more susceptible to ischaemic insults than the grey matter of the brain. Haematoxylin and eosine stained brain slice in

The over the counter medication once known only for its ability of easing aches and pains or fighting off fever and inflammation is proving itself to be quite the miracle drug. Aspirin has become part of the protocol for stroke victims as a preventative measure due to its neuro-protective benefits. Stroke can cause lesions in cerebral white matter, which may result in cognitive impairments such as deficits in learning and memory. White matter lesions (WML) have also been linked to increasing the risk of post-stroke dementia. Cerebral white matter damage has been widely overlooked. Comprised of oligodendrocytes that form the insulating myelin in the CNS, white matter is evidentially just as vulnerable to ischemia as gray matter.