Use Of Neurotrophins On The Function Of The Neuron Signalling Essay

Alzheimer’s is a progressive, irreversible disease that deteriorates parts of the brain, attacking neurons and nerve cells. This results in the loss of important mental functions, especially memory (Alzheimer’s Foundation of America). This disease is detrimental, both to the individual and their friends and family. Alzheimer’s is also a very dangerous disease, as those living with the condition may forget how to drive while operating a motor vehicle, forget where their home is or even forget how to breathe. Not only is Alzheimer’s a progressive and devastating disease, but is also genetic. Research has been pooling out in ways to test individuals for the Alzheimer’s gene – ApoE4 is the genetic variant that triples the risk of developing Alzheimer’s

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.

In 2007 geneticists at National Institute of Aging reports that a genetic risk factor called SORL1 was found in the development of Alzheimer’s (National Institute of Aging, 2008). According to Mattson (2004) mutations in PS1 and PS2 are believed to cause Alzheimer’s by increasing production of the neurotoxin (substance causing damage to nerves) forms of AB (antibody). Along with individuals that inherit E4 isoform (protein) are at increased risk of developing Alzheimer’s.

Some other researchers are trying to determine the possible roles of cholesterol metabolism, oxidative stress (chemical reactions that can damage proteins, DNA, and lipids inside cells), estrogen, vitamin E, and microglia in the development of AD. Scientists also are investigating the role of aging – related proteins (Florida Health Care Association 2005).

From the electronic database searches, several articles were appropriate. The first, "Vitamin D deficiency and depression in adults: systematic review and meta-analysis", was designed to find a relationship between Vitamin D and depression (Anglin, Samaan, Walter, & McDonald, 2013). Although, limited by the lack of random control trials, the data was presented in a uniform and consistent manner (Anglin et al., 2013). The results were in line with their goal, finding that low Vitamin D levels did correlate with increased depression (Anglin et al., 2013). Second, Meehan, and Penckofer, provided their inductive, exploratory opinion of "The role of Vitamin D in the aging adult" (2014). Although, the study was short and depression symptoms were self-reported, it, nevertheless, showed a correlation between low levels of Vitamin D and depression symptoms (Meehan, & Penckofer, 2014). The third article, "Vitamin D supplementation to prevent

As AD is a progressive disease with no currently known cure, all current treatments are aimed at slowing the progression of the disease; these treatments have been available since 1993 (Geldmacher et al., 2011). The desired

(Alzheimer’s Association, 2016). The severity ranges from just memory loss, to the inability to carry a conversation or respond to the environment. That being the case, Alzheimer’s, or Senile Dementia, is an “irreversible and progressive brain disease” caused by the destruction of neurons, and development of amyloid plaques and neurofibrillary tangles in the brain (ADERF, 2016). Scientists have realized through their research with genetics that genes are crucial to the progression Alzheimer’s. Furthermore, the search for genetic variants will help to determine precision medicine, that takes individuals variability in genes, environment, and lifestyle into consideration. (ADERF, 2016). The probability of finding a treatment for Alzheimer's has boomed since the creation of genetic testing. Thus, the stigma that Senile dementia is an “irreversible and progressive brain disease” may soon to be found

AD is a progressive age-related neurodegenerative disorder that poses increasing challenges to the global healthcare system and economic development. AD is characterized by extracellular neurotic plaques composed of Aβ deposits and intracellular neurofibrillary tangles composed of hyperphosphorylated tau with progressive loss of synapses in the brain [1]. Evidence demonstrates a potential link between oxidative stress, mitochondrial dysfunction and AD development [2]. Oxidative damage has been known to occur at a very early stage of AD even prior to Aβ plaque formation and the onset of symptoms [3, 4, 5]. Several cellular changes by oxidative stresses have been related with Aβ plaques formation and pathophysiological events of AD [6].

Moreover, the location of the living place in the world can affect some aspects causing MS to develop, and these aspects are the expose to sunlight and vitamin D concentration in the body (3,5). When people are further away from the equator, they become more in risk to have MS due to decreasing sunlight exposure and vitamin D concentration (5). The relation between sunlight exposure and vitamin D is that sunlight exposure gives the body the essential amount of vitamin D to function properly (3). When Vitamin D concentration decrease, the enzymes that help producing Calcitriol, a substance that helps the brain activate the genes essential for nervous cells to make neurotrophins protein that helps the cells to grow, decrease too causing brain problem

Black has stated that genetic causes often involve the mutation of multiple genes and have identified at least five chromosomes: 1, 12, 14, 19, and 21 (Black, 2009, p. 1894). Four genetic loci have also been identified as contributing to AD, including the amyloid precursor gene, the presenilin 1 gene, the presenilin 2 gene, and the apolipoprotein E gene on chromosome 19. Though there is not enough conclusive research to directly link AD to environmental factors (such as toxins or head trauma) or personal health (diabetes, vascular disease, heart and stroke), these issues are known to contribute to the destruction of brain cells. Understanding the etiology of brain cell loss is relevant to understanding how to effectively prevent the loss of function in the brain. For example, preventing the formation of chemicals called free radicals with antioxidants can indirectly prevent AD. Other causes of brain cell loss include a neurotransmitter called glutamate and an accumulation of beta amyloid proteins. Therefore, although the cause of AD has been unidentifiable, many contributing factors have been observed.

FINDING GENES Causes of AD include extracellular neuritic plaque and intracellular neurofibrillary tangles. The plaque has amyloid-[beta] peptides (Tanzi, 2001). A protein called tau makes tangles

Also, along with Alzheimer’s, there are other diseases such as Parkinson’s which show no improvement and are a huge liability to the health care system. A lot of research is ongoing since ages but no drug is so far available which can cure such a disease. AD occurs due to progressive loss of the neural cells, which causes loss of memory, which might end up as fatal. Recent advances in the research have found the AD occurs to loss of mitochondrial function and mis-folded proteins. Currently six drugs have been approved in the United states for AD. All the drugs have shown moderate improvement in behavioral and functional measures in the

Furthermore, many of the hypotheses have many compelling researched evidences, indicating the cause of AD likely has several influencing factors. Currently, a host of factors including health, environment, lifestyle preferences, and genetics are thought to accumulatively play a role in the development and cause of the disease (About Alzheimer’s Disease: Causes). Anatomical changes within the brains of Alzheimer’s disease patients have produced several schools of thought explaining how they contribute to the disease. For example, neurofibulary tangles, which are twisted fibers of microtubules found in brain cells, are not found in people with normal cognition, but they are found in all Alzheimer’s disease patients. Microtubules are important structures in brain cells which help with the transportation of nutrients and other necessary substances. Another hallmark of AD is Amyloid plaques found in the brain. The plaque is formed from protein fragments forming in between nerve cells. This is thought to inhibit the effectiveness of the brain signals being sent through the nerves and thus impairing cognition. Scientists trying to understand how the formation of neurofibulary tangles and Amyloid plaques occur, have looked at additional signs of AD. These other findings including the integrity of the blood brain

According to recent research, it is believed that Alzheimer’s is caused due to a build up of a protein, called beta-amyloid. This protein peptide is toxic and insoluble, and forms more predominantly in particular regions of the brain, compared to the plaque buildup in a healthy aging person’s brain. Beta-amyloid proteins form from a protein known as amyloid precursor protein (APP), which

BDNF is a member of the neurotrophin family, which includes nerve growth factor, neurotrophin-3, neurotrophin-4/5, and neurotrophin-6 (Poo, 2001). BDNF is broadly expressed in the developing and adult mammalian brain (Poo, 2001), as well as in several peripheral tissues, such as the muscle (Cassiman et al., 2001) and adipose tissue (Sornelli et al., 2009). BDNF plays an important role in various aspects of developmental and adult brain plasticity, including proliferation, differentiation, and survival of neurons, neurogenesis, synaptic plasticity, and cognitive function (Monteggia et al., 2004).