The Pathology Of Alzheimer 's Disease

Alzheimer’s disease known to be a neurological disorder of the central nervous system is an irreversible disorder in which brain cells deteriorate resulting to loss of our cognitive functions, primarily memory, movement coordination, reasoning and judgment, and pattern recognition. In its advanced stage, all memory and mental functioning could be lost (Healthcommunities.com, 2016). This disease is known to be caused by parts of the brain shrinking (atrophy), which destroys the structure and function of particular areas of the brain (Nhs.uk, 2016). Although the exact cause to this process is not known, research suggest that in the brains of patients with Alzheimer 's disease, scientists have found amyloid plaques (abnormal deposits of protein), neurofibrillary tangles containing tau and acetylcholine a chemical imbalances (Nhs.uk, 2016).

They studied this drug over the course of two months by comparing a group of normal mice to two groups that have been engineered to emulate symptoms of Alzheimer’s such as the memory loss and presences amyloid plaques in the brain among others. One of these groups was treated with the TA while the other was not.

Alzheimer 's disease (AD) is a progressive degenerative disease of the brain from which there is no recovery. There are three brain abnormalities that are the hallmarks of the Alzheimer’s disease is initially caused by plaques buildup in the brain’s neurons as illustrated in figure 1. The support structure that allows the flow of the nutrients through the neurons gets damaged and ultimately there is loss of connection among the neurons and they die off (National Institute of Health, 2015). This causes the brain tissue to shrinks, which is called atrophies. All this ultimately lead the victim of this disease to face difficulties in governing emotions, recognize errors and patterns, coordinate movement, and remember. Ultimately, a person with AD loses all memory and mental functioning.

Alzheimer’s disease is a chronic neurodegenerative disease that accounts for sixty to seventy percent of Dementia cases. It is characterized by the development of amyloid plaques and neurofibrillary tangles, the loss of connection between neurons in the brain and the death of nerve cells. There are two types of Alzheimer’s Early on-set Alzheimer’s which occur from the ages of thirty to sixty is very rare and makes up less than five percent of the cases of Alzheimer’s . The second type is Late on-set Alzheimer’s which is the most common type and it is found in those of ages sixty and up. The progression of Alzheimer’s is a lengthy progress from the time of diagnosis the average life expectancy is three to nine years. In the early stages people have difficulty with short term memory loss as the disease progresses symptoms include difficulties with language, disorientation, mood swings, loss of motivation, loss of self-care and behavioral issues. As Alzheimer’s progresses a person slowly withdraws from family life and society due to the jumbled state of their memory. On a physical level the body’s physical function slowly degenerates and eventually leads to death.

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

Cognitive impairment associated with Alzheimer’s disease occurs when synapses, which transmit information from one neuron to another, become interrupted and communication ceases (7). The result is death of the nerve cell within the brain, also referred to as synaptic failure (6). Synaptic failure takes place when amyloid plaque and neurofibrillary tangles develop (7). Amyloid plaque develops from amyloid beta proteins, which are released by enzymes from the amyloid precursor protein that is located on the surface of the neuron (7). The amyloid beta proteins are normally cleared within the body once they are released however, in

Some physicians also prescribe high doses of vitamin E for cognitive changes. The most common treatments today are cholinesterase inhibitors (FDA-approved drug), memantine (FDA-approved drug), vitamin E, and many alternative herbal treatments including caprylic acid, coconut oil, and coral calcium. With all of the treatments out there though, it is difficult to discern which is the best one. The purpose of this paper is to compare and contrast the different treatments available today in order to find the best line of treatment for AD. In order to do so, we will be looking at the efficacy, side effects, cost effectiveness, availability, dosage, and those most likely to benefit from each treatment.

The first is Donepezil. The drug is very potent and it works by inhabiting AChE , the important neurotransmitters (Hodis, 2014). The drug helps reverse the decrease in brain function (Hodis, 2014).

Cholinesterase inhibitors are used to breakdown the acetylcholine, which is a neurotransmitter that is connected to memory, by blocking the enzyme acetylcholinesterase. The donepezil, rivastigmine, and the galantamine are three commonly prescribed cholinesterase inhibitors. The known side effects are nausea, vomiting, diarrhea, upset stomach, and dizziness (Wattmo, Londos, & Minthon, 2014). To block the NDMA receptors, the memantine is prescribed to improve cognition and regulate the glutamate that acts as a neurotransmitter in the brain around the learning and memory area. Excessive glutamate could cause damaged, killed nerves. Common side effects of memantine consist of dizziness, confusion, and headaches (Koch, Szecsey, & Haen, 2004). Additional medication can be prescribed to patients with symptoms such as depression, psychosis, disturbed sleep, and apathy. Howes (2014) supported the commonly used drug treatments as he compared AD to the issues of the cardiovascular disease. The reduced blood flow to the brain, the reduction of oxygen, clogged arteries and vessels could damage the brain cells, making the Alzheimer’s disease worse. The treatment of AD reduces some of the effects of the cardiovascular (Howes,

The first ones are Cholinesterase inhibitors which communicate nerve cells and postpone deterioration for six

The pathology of Alzheimer disease could be affected by many factor for example G6PD play a critical role in the progression and/or the prevention of this disease.

5 When consuming 24 mg/day (0.34 mg/kg/day) for 56 days, five volunteers displayed reduced cholinesterase activity two weeks after the dosing began. A maximum cholinesterase inhibition of 25% was observed three weeks after the end of the dosing period

Many articles and journals have been published about this drug receptor and preclinical data summarizes the efficacy of 5HT6 receptor antagonist in cognitive function. Growing number of patent in protecting 5HT6 chemical entities have been successfully endured phase I clinical studies and clinical phase II trials. It is likely that the combination of 5HT6 receptor antagonist and cholinesterase inhibitor have also been revealed after phase II studies. Then two of these antagonists have been taken for further studies phase three clinical trials. To sum up 5HT6 receptor antagonist is regarded as one of the potential and promising drug candidate to treat Alzheimer’s disease. (Ferrero. H., Solas. P., Maria. Rairez.J. (2017)

Acetylcholine is formed by neurons termed as cholinergic neurons. In the external nervous system, acetylcholine plays a vital part in skeletal muscle movement, as well as in the adjustment of smooth muscle and cardiac muscle. In the central nervous system, acetylcholine is understood to be involved in learning, mood and memory. It carries nerve impulses through a gap called a synapse; there it circulates nerve impulses in the receiving neuron. The well-known Alzheimer’s disease is caused by the decrease of this certain neurotransmitter, for this reason when treating it medications which contain acetylcholine are taken. Individuals with reasonable levels of dementia can display noticeable improvement with this sort of treatment. A supporting study by Martinez and Kesner (1991) depicts the significance in memory development. Rats were qualified to go complete a maze, where they were given food at the finish line. Once the rats had trained enough to do this, they were divided into three groups: group 1; rats were injected with a chemical that reduced the levels of acetylcholine, group 2; rats were injected with an enzyme that increased their levels of acetylcholine and group 3; the control group, which were given no form of injections. Results culminated that rats in group 1 were slower at finding their way making more errors than both groups 2

temporarily help memory and thinking problems in patients. (7, p.1046). Additionally, the effectiveness of these drugs varies between patients (3). According to the Alzheimer’s Association there are several promising new drug therapies in the development stages that may be more effective in stopping the disease progression and ultimately curing Alzheimer’s patients. Two drugs, in particular, in the research stage, show exciting potential. The first, Solanezumab, is designed to lower the levels of beta-amyloid in the brain thereby stopping the damaging plaques from adhering to brain tissue. The second, CSP-1103, is a microglial modulator that targets inflammation in the brain and also works to prevent beta-amyloid from being deposited on brain tissue (3).