Magnolia Officnali And Bark Essay

Plaque deposits are clumps of protein and dead cells in the grey matter as well as along blood vessels within the brain. Intracellular flaws have been found in nerve cells of Alzheimer’s patients, such as mutations in the cell structures that make them unable to change genetic information into proteins, a step that is necessary for memories to be stored. A major factor appears to be chemical imbalances caused by lack of enzymes needed to make chemicals for transmitting information from one cell to another. It is unknown how these defects are interrelated, and more study needs to be done to determine the connections and causes. If Alzheimer’s disease was given more attention in the public eye, that would stimulate more medical research to determine how the disease works and maybe even point to prevention or a cure.

A great number of patients with Alzheimer’s disease have less amount of Acetylcholine in the cerebral cortex. Acetylcholine function is for the cognitive activity of the brain. A big amount of neuritic plaques in the cerebral cortex found in brain of a Alzheimer’s patient. Beta amyloid is a type of protein that engage the center of the plaques that destroy the neurons that provide Acetylocholine (Ach) that are necessary element for learning and memory process. The brain of a person with Alzheimer’s shows marked with atrophy, widened sulci and shrinkage of the gyri. Majority of the most cases, every part of the cerebral cortex is involved, but the occipital pole is save from strain. The cortical ribbon may be reduced and ventricular dilatation visible, especially in the temporal horn, due to atrophy of the amygdala and

In addition, decreased cerebral blood flow, environmental toxins and a decrease in acetylcholine have all been labeled potential culprits. Various theories for the cause of Alzheimer’s have been put forth but as yet none have been shown true.

The human body has a built in stress response system that usually self regulates. When a threat is perceived the body deploys white blood cells to the area of the body that is under attack (Segerstrom & Miller, 2006). Because of this, less important cellular activities are reduced and the immune system is left vulnerable. When the body perceives a threat there are three phases it goes through. (Story, 2012). The first is the alarm stage, in which the sympathetic nervous system is stimulated and in response deploys the release of

The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain

Earlier research was done on the inhibition of amyloid β, but a relatively new approach is to find inhibitors for acetlycholinesterases enzyme (AChE). The action of AChE results in the blockage of transmission of acetylcholine (ACh), hence hyperphosphorylating the tau protein which affects the breakage of amyloid precursor protein(APP), which firther results in the increase in amyloid β. The binding of AChE causes decrease in the binding of ACh to muscarinic recptor and nicotinic receptors (Francis, Palmer, Snape et al., 1998). A recent study has shown that ACh does not only have cognitive functions, it regulates the

Alzheimer’s is a type of dementia that causes complications with memory, thinking, and behavior. Long before any signs of memory loss, there a microscopic changes occurring in the brain, altering its functionality (Alzheimer 's Association Organization, 2016). The brain has billions of nerve cells that work together, and when one portion of the brains neurons are malfunctioning it leads to breakdowns in other parts of the brain. The two most noted abnormal structures that are suspected to damage and kill neurons in the brain in patients with Alzheimer’s are plaques and tangles. Plaques are deposits of a proteins fragment called beta-amyloid that build up in the spaces between nerve cells; and tangles are twisted fibers of another protein called tau that build up inside cells (Alzheimer 's Association Organization, 2016).

Although at this age it effects only about 1 in every 1,000 individuals, by the age of 80, this statistic drastically elevates to 1 in every 5. It is still unclear what causes this deterioration of the brain, and why its decline correlates so strongly to age. However, many different theories have been developed such as the ‘Amyloid Cascade Hypothesis.’ Alzheimer’s disease is currently irreversible, and causes visible differences in brain tissue. The brain contains a protein called tau; it congregates in both the white and grey matter of the brain, forming tau tangles. Irregular protein called plaques are also found in the brain; these emerge when different protein gets sliced up by an enzyme in the fatty membrane surrounding nerve cells, resulting in clumped beta-amyloid proteins forming plaques. These impede cell-cell signalling between neighbouring neurons. The result of this is a loss of function including the synthesis and processing of vital neurotransmitters, for example dopamine. Plaques and neurofibrillary tangles work together to deform the brains structure, block signalling and communication between cells, and trigger immune reactions

In individuals with Alzheimer 's disease, the cells that create acetylcholine are harmed or killed and levels of the chemical slowly decrease in the brain. (alz.org)

Alzheimer’s is a progressive brain disorder characterized by problems with memory, reasoning, behavior and motor skills. Alzheimer’s is the most common form of dementia and its symptoms develop slowly and get worse over time ("Alzheimer's Disease | AD | MedlinePlus," 2014). In Alzheimer’s disease, a patient’s brain cells begin to degenerate and eventually die, causing a severe decline in memory and mental function; making it nearly impossible for a patient to perform daily tasks. Although the causes of Alzheimer’s are not fully known, scientists believe that it is “caused by a combination of genetics, lifestyle, and environmental factors that damage the brain over time” (Mayo Clinic Staff , 2015).

This research report will provide a general overview of Alzheimer’s disease. This overview will include background and history of the disease dating back to its discovery by Alois Alzheimer in Germany. It will provide in-depth information on the anatomy and pathophysiology of the disease, specifically on the roles of beta-amyloid plaques and neurofibrillary tangles and on how they progress; what happens as they progress through the brain. Other topics that will be briefly covered include etiology, epidemiology, treatment, and prognosis.

Supporting 1.1 : Babbler’s Bill Leaf effective for allergies antioxidant. She said that Babbler’s Bill Leaf can protect the liver which is organs that eliminate toxins. This is a mechanism to save the patient’s life.

Echinacea (Echinacea purpurea) is one of the nine species in the Asteraceae/Compositae family, related to the daisy. The North American origin gives insight to its first use in Native American herbal medicine. The plant is commonly used in minor respiratory infection remedies and labeled as a functional food for its properties in increasing antibodies when served in as an herbal drink or pill. Further analysis of this functional food will give light to the common sources, clinical description and side effects drawn from studies to date.

Alzheimer’s disease is a neurodegenerative disorder characterized by the loss of memory and other cognitive abilities essential for the function of a healthy human being. Neuropathologically, the disease is characterized by the presence of neurofibrillary tangles and senile plaques, impaired synaptic function and cell loss.1 There is a major loss of cholinergic, noradrenergic, and dopaminergic neurons while at the same time there is an accumulation of free radicals and oxidative stress, leading to lipid peroxidation and neuronal degeneration in the tissues of the brain. Not only are there major physiological changes in patients with Alzheimer’s disease, but with these changes come cognitive symptoms as well. These include disruptions in memory, language, thinking,

IThe potential therapeutic properties of T. arjuna have been reported extensively in traditional medicine system and have been evaluated by various in vitro and preclinical studies with the aim of characterising various pharmacological activities (Table 2). Some studies have reported that the saponin glycosides content of T. arjuna might be responsible for the inotropic effects, while the flavonoids provide free antioxidant activity as well as vascular strengthening, conforming the pleiotropic actions of T. arjuna (Figure 3). Although, voluminous data is available from the various preclinical experiments on T. arjuna, but a unifying hypothesis that accounts for its biological activity and targets are still unidentified and under discussion.