Effect Of Resveratro

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

Lab research has suggested that resveratrol might have some powers against the diseases of aging -- including Alzheimer's disease. But evidence from human studies has been lacking.

Resveratrol (3,4 ',5-trihydroxystilbene) is a naturally occurring phytochemical present in red wine, grapes, berries, chocolate and peanuts. Clinically, resveratrol has exhibited significant antioxidant, anti-inflammatory, anti-viral, and anti-cancer properties. Although resveratrol was first isolated in 1940, it was not until the last decade that it was recognised for its potential therapeutic role in reducing the risk of neurodegeneration, and Alzheimer 's disease (AD) in particular. AD is the primary cause of progressive dementia. Resveratrol has demonstrated neuroprotective effects in several in vitro and in vivo models of AD. Apart from its potent antioxidant and anti-inflammatory roles, evidence suggests that resveratrol also facilitates non-amyloidogenic breakdown of the amyloid precursor protein (APP), and promotes removal of neurotoxic amyloid beta (Aβ) peptides, a critical step in preventing and slowing down AD pathology. Resveratrol also reduces damage to neuronal cells via a variety of additional mechanisms, most notably is the activation of NAD+-dependent histone deacetylases enzymes, termed sirtuins. However in spite of the considerable advances in clarifying the mechanism of action of resveratrol, it is unlikely to be effective as monotherapy in AD due to its poor bioavailability, biotransformation, and requisite synergism with other dietary factors. This review summarizes the relevance of resveratrol in the pathophysiology of AD. It also highlights

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 sub-acute phase continues from the acute phase and characterized by new events such as formation of free radicals, delayed calcium influx, apoptotic cell death, inflammatory response, central cavitation initiation, and astroglial scar initiation (28). Neutrophils are the first immune cells to respond/arrive at injury, removing microbial intruders and tissue debris. Neutrophils release protease metalloproteinase, ROS, TNF-α, IFN-γ, IL-1, 8, 12 and other pro-inflammatory factors to activate other inflammatory and glial cells (29, 30). While initially beneficial, neutrophil persistence significantly increases damage through continuous production of pro-inflammatory cytokines and proteolytic enzymes (31). Therefore, neutrophil activation is limited to a couple days, and is contained to the sub-acute phase. Microglia and macrophages become active in response to neutrophils and the injury, also releasing numerous

Curcumin has been proven to help recover from neurodegenerative diseases, even aiding in their prevention, and inhibiting inflammatory molecules in the brain (Petraglia, et al., 2011, p.4). Foods high in curcumin include Indian curries, yellow rice flavored with turmeric, and mustard (Curinga 1). Caffeine, although showing mixed results in some studies, shows reductions in neurological deficits (Petraglia, et al., 2011, p.8). One of the best high caffeine options is green tea at a recommended three cups per day (Maroon, et al., 2011, p.6). As seen in some research on green tea, the result of its high consumption in Asian countries leads to the “Asian paradox,” or the significant prevention of neurological problems in Asia (ibid). Vitamin E in nuts, seeds, vegetable oils, and cereals has been tested to show improved cognitive performance, improved spatial memory, and less neuropathology (Petraglia, et al., 2011, p.9). Vitamin E intake is improved in conjunction with Vitamin C (ibid). Foods high in Vitamin C include citrus fruits, tomato juice, and potatoes (“Office of Dietary Supplements – Vitamin C,” 2016, p.2). Finally, Omega 3 has been consistently shown to help in recovery from PCS and inflammation (Maroon, 2011, p.1). They are the most effective natural anti-inflammatory food and has been tested to be neurotherapeutic for PCS (Maroon et al., 2010,

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.

Colton et al. (2014) research looked at 117 clients who experienced increase intracranial pressure as a result of severe traumatic brain injury. Their research looked at client’s respond to pharmacological interventions and these pharmacological interventions include hypertonic saline, mannitol, propofol, fentanyl, and barbiturate. In their research Colton et al., (2014) found “all treatment resulted in significant intracranial pressure changes after 1 hour or 2 hours except for mannitol and barbiturate administration” (Colton at el., 2014). This finding is significant given that mannitol is used as a first line treatment for management of increased intracranial pressure. The chart below demonstrates how each of these pharmacological interventions decreased intracranial pressure and it allows us to compare each pharmacological intervention to each other. (Colton et al., 2014)

Traumatic brain injury affects people from all walks of life. Form military personal to the elderly that get injured when they fall or even athletes in relation to the injuries they acquire. Traumatic brain injury progressively leads to complex pathophysiological events that may lead neurodegenerative complications. For those that have experienced traumatic brain damage are more susceptible for the development of diseases such as Alzheimer’s, dementia, epilepsy, posttraumatic stress disorder, and neuropsychiatric disorder. The progression of these diseases can occur in a span of a few weeks, months, or even decades after trauma, so it is important to look over the underlying pathophysiology that traumatic brain injury can cause after the injury

2010). The neuroinflammation is an early, non-specific immune reaction to tissue damage or pathogen invasion (Lee et al. 2010). Inflammation of the central nervous system (CNS) is characterized by increased glial activation, pro-inflammatory cytokine concentration, blood-brain-barrier permeability, and leukocyte invasion (Lee et al. 2010). Microglia are cells that support and protect neuronal functions (Lee at al. 2010). They act as the first and main form of active immune defense that orchestrate the endogenous immune response of the Central Nervous System. The microglia play a central role in the cellular response to pathological lesions such as Aβ. Aβ can attract and activate microglia, leading to clustering of microglia around Aβ deposits sites in the brain (Lee et al. 2010). Even though microglia have neuroprotective functions, neurotoxic mechanisms which involves continuous activation of microglia and toxic factors are released by microglia, which may lead to neuroinflammation (Lee et al. 2010). Astrocytes (star-shaped glial cells) are the most abundant cells in the brain and are located in the brain and spinal. Astrocytes have various functions such as: biochemical support of endothelial cells of the BBB, supplying nutrients to the nervous tissue, maintenance of extracellular ion balance, and healing the brain and spinal cord following traumatic injury (Lee et al., 2010). Chemokines are released by astrocytes which attract microglia and they further express proinflammatory products, thus increasing neuronal damage in the pathogenesis of AD (Lee et al., 2010). Astrocytes play a critical role in Aß clearance and degradation, and they also provide trophic support to neurons forming a protective barrier between Aß deposits and neurons (Wyss-Coray et al., 2003). Neurons contribute to the production of

It is a well-known biomarker of brain injury associated with Alzheimer’s disease, concussion and epilepsy. Based on literature review, an overproduction of soluble S100B from the astrocytes binds to the receptor for advanced glycation end products (RAGE) leading to various responses including increased reactive oxygen species (ROS) formation, release of pro-inflammatory markers, and activation of stress response kinases resulting in neuronal cell death. The ongoing neuronal injury and inflammation further promotes cellular apoptosis and impairs neurogenesis in epileptic brain. Identification of this mechanistic relationship between acquired epilepsy and inflammation will provide an important therapeutic target pathway for prevention of

Emerging evidence indicates that free radicals are involved in the pathogenesis of several digestive system disorders as well as in the regulation of biological processes such as aging. Previous reports have indicated that opioids induce apoptosis via stimulating an oxidative stress pathway that is associated with the production of superoxide and nitric oxide (NO) [11]. NO, together with reactive oxygen species (ROS), has a pivotal role in the regulation of apoptosis and necrosis in various cells. Hsiao et al. investigated the role of NO and ROS in the morphine-induced apoptosis. They found that the morphine treatment enhanced apoptosis through both NO and ROS pathways [12]. The inducible nitric oxide synthase (iNOS) enzyme is one of the most important enzymes involved in the generation of NO from the amino acid L-arginine.

Also known as polyunsaturated fatty acids (PUFAs), Omega-3s play a critical role in brain function and in normal growth and development.

The BBB evolved as an extremely tight barrier to protect the brain from potentially toxic compounds. Though it is an indispensable part of the Central Nervous System, its tightness makes delivering therapeutic drugs to the brain very difficult.

     The blood brain barrier protects brain cells from harmful substances, as well as, pathogens, by preventing passage of many substances from blood into brain tissue.