Alzheimer's Disease Essay

Alzheimer's and dementia is one of the many diseases that affects the nervous system, particularly the brain. Acute memory loss is known as dementia. Thus, Alzheimer's is a severe form of dementia. The diagnosis is the brain lacking brain cells and connections due to degradation. Symptoms of Alzheimer's includes memory loss which can range from minor to severe as well as confusion which directly corresponds to memory loss. Groups of nerves work together to focus on specific jobs such as communication and memory. The brain cells work together and “receive supplies, generate energy, construct equipment and get rid of waste.” Alzheimer's is believed to prevent parts of the cell to not function properly. Scientists are not thoroughly sure where the cells malfunction begins. As the cell continues to divide and spread, the infected cells begin to die off leading to damaged brain connections. Scientists believe that plaques and tangles are the cause of the disease. Plaques are “deposits of a protein fragment called beta-amyloid that build up in the spaces between nerve cells.” Tangles are “twisted fibers of another protein called tau that build up inside cells.” Age results in developed plaques and tangles though, Alzheimer patients have an abnormal amount of these

Autosomal dominant mutations in APP, PSEN1, or PSEN2 that alter APP processing and the production or self aggregation of Aβ, promote aggregation and accumulation of Aβ in brain causing early-onset AD (Bertram et al., 2010).

Alzheimer’s disease is the most common form of dementia and is characterized by the degeneration and death of brain cells that causes a loss of mental function. Although neuronal loss is not considered a normal part of aging, age is a significant risk factor for Alzheimer’s disease (AD) (Lindsay et al., 2002). Hallmarks of AD include tau tangles and Amyloid-β plaques, whose interaction is thought to lead to neuronal death (Ittner & Götz, 2011). At present, there is no singular cause identified for AD, and further study is required before a cure can be developed. One proposed link to AD is a mutation in Microtubule Associated Protein Tau (MAPT), coded by the MAPT gene located on chromosome 17 (Lee, Goedert, & Trojanowski, 2001). Tau protein is normally soluble and functions to stabilize microtubules within axons. However, mutations in MAPT can cause Neurofibrillary Tangles (NFTs) comprised of hyper-phosphorylated tau protein to collect within neurons and spread throughout the brain (Clavaguera et al., 2009). These tau tangles are detergent-insoluble and impair axonal transport to an extent (Zhang et al., 2012). Transgenic mice expressing mutant human P301S tau protein exhibit synaptic dysfunction followed by hippocampal and cortical neuronal loss (Yoshiyama et al.,

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

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

Subsequent studies in animal models for insulin resistance, AD, or both, have established that insulin resistance exacerbates Aβ and tau phenotypes including enhanced Aβ 42/40 ratio, total tau, and hyperphosphorylated tau (Ho et al., 2004; Lester-Coll et al., 2006; Li et al., 2007; Masciopinto et al., 2012; Plaschke et al., 2010; Qu et al., 2011; Searcy et al., 2012; Takeda et al., 2010) and AD amyloidosis models exhibit insulin resistance (Rodriguez-Rivera et al., 2011).

Scientists believed in 1995 that there was a genetic influence in over half the cases of Alzheimer's disease. The gene scientists are giving the most consideration to apolipoprotein E gene (ApoE) as the main gene involved in the development of Alzheimer's disease. Everyone has this gene; if they did not, they would not be alive. ApoE carries a person's cholesterol through their blood. The effect that this gene has in terms of the brain is not totally understood. Scientists have found that

The disease called Alzheimer’s is the fourth leading cause of death in the United States (Weiner, 1987). It is estimated that the elderly population will double between now and 2030. During this period, the number of elderly will grow by an average of 2.8% annually (U.S. Census Bureau, 2001). By 2050, the number of people with Alzheimer’s is estimated to range from 11.3 million to 16 million (Alzheimer’s Association, 2005). These startling numbers should prompt an examination into one of the leading causes of death among this group of people. Understanding what Alzheimer’s is and the known causes of the disease are a good starting point. For those who have aging family members, knowing the risk factors and warning

Alzheimer’s disease (AD) is a complex and multifactorial neurodegenerative disease and the most common cause of dementia. Finding the potential genes involved in AD is an essential step in molecular diagnosis and is important to understand the mechanisms leading to neurodegeneration. The genetics of early-onset AD (EOAD) are largely understood with mutations in three different genes. In contrast, the genetics of late-onset Alzheimer’s disease (LOAD) are not fully understood. LOAD is much more common and far more complex than EOAD because of the involvement of numerous genetic, epigenetic and environmental factors. The apolipoprotein E (APOE) ε4 allele has been found to be a main risk factor for LOAD. Genome-wide association studies (GWASs)

The mean onset age of AD is 84.3 years, compared to 75.5 years for subjects with one APOE-4 allele, and 68.4 years for subjects with two APOE alleles. (Corder 1993) While this study was relatively small with just shy of 250 participants, all relevant assertions are backed by statistically significant analysis. It is important to note, however, that a large portion of participants in the study did not have an APOE-4 allele, which suggests other genetic sources of risk exist. Nonetheless, the study depicts strong evidence of the direct link the APOE-4 allele has on AD. Although APP mutations and APOE-4 alleles don’t account for all genetic AD cases, they have led to the discovery of 21 genetic loci that also impact AD. (Guerreiro, 2013) This has narrowed the focus of scientists and allowed them to make advances in continuing to study the link between genetics and AD.

A growing body of evidence has indicated that sAD is multifactorial, with age being an important risk factor. Main neuropathological hallmarks identified in Alzheimer’s brains are beta-amyloid deposits, hyperphosphorylated tau proteins, and astrogliosis [1]. Recently, dysregulated brain insulin signaling has been reported to play a pivotal role in AD pathology. Additionally, several studies have indicated that insulin malfunction induces beta amyloid accumulation and tau pathology in AD brain [2]. Thus, Alzheimer’s disease has been argued to be a type III diabetes [3, 4]. Given the specific nature of sAD, there is no clinical evidence on its early stage, and this makes making an appropriate model more difficult. Thus, a convenient model for the initiation phase of sAD could be the

The Journal of the American Medical Association reports the latest break through in the study of gene causing Alzheimer’s has pointed to two genes, chromosomes 2 and 19 that cause the disease (7). The article also points out another gene, A polipoprotein E-e4, is also linked to Alzheimer’s disease. According to the Journal of Alzheimer’s disease, Jose Vina and Ana Lloret writes that women are at higher risk of Alzheimer’s due

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by β-amyloid plaque formation caused by aggregation of β-amyloid42 within the brain leading to a progressive decline in cognitive function and memory loss (2). Hyperphosphorylated tau protein is occasionally found in brains of AD patients with advanced pathology however, it is not necessarily an indicator of AD but considered a sign of disease severity (2, 4, Kosik et al, 1986). AD is separated into two subcategories following the simple sporadic and familial disease classifications, early-onset AD (EOAD) which develops in individuals between 30 and 60+ years of age and late-onset AD (LOAD) which develops in individuals 60 years of age or older (2). Familial AD may

Till date, the molecular mechanisms associated with AD have remained elusive and no drug can reverse the pathological process [265]. Since the clinical diagnosis of AD is currently based on qualitative often subjective, the need for a sensitive, specific and reliable markers to diagnose and monitor the disease progression in AD is essential. The biomarkers evaluated to date, including CSF levels of total tau, phosphorylated tau and amyloid-β₄₂ (Aβ₄₂) unfortunately have not shown the accuracy and reliability

In late onset Alzheimer's case, the genetic test involves a simple blood test, revealing whether the patient has apolipoprotein E (APOE) alleles, which may increase the risk of Alzheimer's onset. There are three types of APOE alleles: E2, E3 and E4. The E2 allele has shown a reduced risk of late onset Alzheimer's. The E3 allele is the most common and has no effect on chances of having alzheimer's. On the other hand, the E4 allele increases the