Molecular And Cellular Mechanisms Of Toxicity And Cancer

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).

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.

Alzheimer’s is caused by broken signals within the brain leading to the death of brain cells, this can also lead to a shortage of some important chemicals, these chemicals control the transmitting of messages to the brain.

Arsenic has been shown to cause cancer and deaths. However, the element is multifaceted because in other studies it has been shown to have a healing effect. Be that as it may, the component is clearly exceptionally equivocal in light of the fact that in different reviews it has been appeared to have a recovering impact.

While aluminum has been to be a neurotoxin, the fact that it could be a cause of Alzheimer becomes evident in the case of a 58 year-old Caucasian male who worked with the preparation of a material, "DARMATT KM1 that was used as insulation in the nuclear fuel and space industries"(Exley, 2). This indicates that he was exposed to " aluminum sulphate 'dust' ona daily basis over 8 years." The Caucasian male eventually died at the age of 66, after multiple complaints of "headaches, tiredness and mouth ulcers." This man's frontal lobe was then cut into fifty pieces each weighing approximately 300mg, this sample confirmed that this man had a extremely high dosage of aluminum in his frontal lobe alone and while it does not prove that it caused Alzheimer's to appear it does indicate that aluminum was highly likely to have contributed to the rapid progression of the disease. There have been many more theories as to what causes the degenerative disease; Oxidative stress which occurs when the body creates too many free radical and their is an imbalance of available antioxidants then damage can occur. Amyloid Proteins can also be named for contributing to the growth of Alzheimer's, such proteins as AB, tau, and oligomers can be "the real culprit in the neurotoxicity that is the characteristic of AD' (Shan 35).

Alzheimer’s disease is named after Dr. Alois Alzheimer who first discovered deviations from normal tissues of healthy individuals in the brain tissue of a lady in 1906. The woman, who showed symptoms of erratic behavior, loss of memory, and problems with communication, died of a then unfamiliar mental disorder. This led Dr. Alzheimer to investigate the cause of her unusual death. He assessed the brain of the woman and found that there were many anomalous masses (amyloid plaques) and intertwined bundles of fiber (neurofibrillary tangles). Scientists today have pinpointed the qualities of Alzheimer’s to be a) tangles in the brain (neurofibrillary tangles), b) plaque in the brain (amyloid plaques), and c) loss of connections among nerve cells.

Scientists are not entirely sure but they think it could be a protein ApoE in the blood, but the most obvious cause they can find is tangled nerve cords . Apoe is a protein that moves cholesterol in the blood. Scientists also hypothesize that genetics are a higher risk ("Alzheimer's Disease Information: Facts, Causes, Definition, and More").

Alzheimer Disease, the most common form of dementia (to a group of symptoms affecting the brain), is a neurological disorder affecting an individual’s memory, thinking skills, and ability to conduct simply everyday tasks. Alzheimer Disease is irreversible, and no cure has been established. Dr. Alois Alzheimer-the individual in which the disease is named after-detected Alzheimer in 1906 from a woman with abnormal clumps and tangled neurofibrillary (Castellani 2010). These characteristics of the brain are now directly associated with Alzheimer Disease. There are essentially two forms of the disease. Both experience the same symptoms, but one is early onset and the second is late onset. In early onset Alzheimer Disease, symptoms develop as early as 30 years of age. Late onset AD, the most common form, develops at sixty years of age and older. A family history of the disease does improve the individual’s probability of experiencing symptoms. The progression of this paper will consist of the medical changes caused by Alzheimer, how an individual can obtain it, and lastly prevention methods discovered throughout the years.

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

Alzheimer’s is a disease which affects the brain. Being completely irreversible, a person’s memory, thought process, and motor skills become drastically challenged, and eventually taken away. Symptoms will usually appear in subjects around age 60, however, signs have been known to start much earlier. Drastic changes can also occur with the brain, visibly shrinkage occurs, and neurons slowly cut off from each other, and die. In addition to this, unnatural formations of proteins begin forming on the brain. (ADFS)

ALD affects the nervous system in the brain. The disease strips away the coating or the

The research into Alzheimer's Disease has come a long way since 1906 when it is was discovered by Alois Alzheimer. He detected microscopic brain tissue changes called senile and neuritic plaques in deceased patients. These are chemical deposits consisting of protein molecules called Amyloid Precursor Protein(APP) that are fundamental components of a normal brain. However in the brain of an Alzheimer patient, an enzyme cuts the APP apart and leaves fragments in the brain tissue. These combined with degenerating nerve cells cause the plaques or lesions. These lesions are found in many sections of the brain including the hippocampus which regulates emotion and memory, the basal forebrain, and especially the basal nucleus of Meynert and the cortex, where the memory function is located.(2) Another sign of a diseased brain are neurofibrillary tangles, which are malformations within nerve cells.

Here they concentrate more on the iron and aluminum mass in the hippocampus. According to this studied the Alzheimer’s disease has similar symptoms to dementia pugilstica .Patients with punch drunk (dementia pugilistica) showed sign such as aggressive behavior. The similarities between the syndromes between Alzheimer’s disease and Punch drunk, and also between the deficits may suggest that this two diseases have similar etiological mechanism which means the reasons caused these two are the same. The symptoms such as having an aggressive behavior is explained by having smaller amount of Purkinje cells, also ventricles are becoming bigger than normal size. The reason for those symptoms are repetitive brain injuries in case of boxing getting repetitive hits on the heads of boxers. Bur the most important problem in punch drunk syndrome is that neurofibrillary tangles (NFT) are being developed. The statement about NFT again brings to the ide about similarities between Alzheimer’s disease and punch drunk syndrome but there is difference between distributions of it in both cases. In AD (Alzheimer’s disease) it has been seen in deeper levels. But however NFT had higher level of Al and Fe in punch drunk syndrome than in Alzheimer’s

However, some scientific studies show that Alzheimer disease occurs when nerve cells in numerous key areas of the brain are destroyed or damaged. The damaged or destruction of these nerve cells in the brain disrupts the information flow between the body and the brain. This disruption leads to a stable decline of both mental and physical functions. Scientists say that the destruction of the brain is most likely to be caused by the development of senile plaques (clumps) and neurofibrillary tangles (knots). These plaques and knots are usually found on the brain of a diseased person during after death biopsy. They are mostly found on the part of the brain that is associated with the memory and retention of information (National Institute Of health 10).

and Mattson, 2011), and impairments of axonal transport and mitochondrial functions (Decker et al., 2010; Querfurth and LaFerla, 2010; Sheng and Cai, 2012). In addition, several lines of evidence suggest that Aβ regulates neuronal and synaptic activities and that its accumulation in the brain causes aberrant network activity and synaptic depression (Palop and Mucke, 2010). Impairments of inhibitory interneurons and aberrant stimulation of glutamate receptors result in excitotoxicity, and play important upstream roles in this pathogenic cascade. These impairments also lead to a positive feedback loop, where aberrant neuronal activity augments Aβ production, which in turn leads to further neuronal damage (Palop and Mucke, 2010; Bero et al., 2011; Verret et al.,