Fully detailed pharmacology around AlZheimer’s disease and what genetics involved ? Essay Example

Medicine

Fully Dеtаilеd Рhаrmасоlоgy arоund Аlzhеimеr’s Disеаsе and the Gеnеtiсs invоlvеd

Pharmacology around Alzheimer’s disease

Researchers have not identified a drug treatment for Alzheimer’s disease. However, there are various medicines that are developed to momentarily lighten the disease symptoms, or slow the progression of the disease (Sassy et al., 2016). There has been a development of many drugs. These drugs have both the generic and brand name. Two major types of drugs that treat AD include; acetylcholinesterase inhibitors and NMDA receptor antagonists. However, the generic name for acetylcholinesterase inhibitors includes rivastigmine, donepezil, and galantamine (Frampton, 2014). Initially copyrighted as the trademark name Aricept, Donepezil is extensively obtainable as standard donepezil. Copyrighted as Exelon, Rivastigmine is accessible as other trademarks and as universal rivastigmine as well. Galantamine, initially patented as Reminyl is available in its generic form, galantamine as well as brands such as Remyl Xl, Gatalin XL, and Acumor XL. The NMDA receptor antagonist is memantine and was previously copyrighted as Ebixa. Currently, the drug is offered as generic memantine. Maruxs and Memantine are other UK brand names.

The brain of an individual suffering from AD is characterized with acetylcholine which assists in sending information between the nerve cells. Low acetylcholine levels are linked to worsening AD symptoms. The acetylcholinesterase inhibitors prevent acetylcholinesterase enzyme from breaking down acetylcholine. The results is increased communication between the nerve cells, hence a temporal stability of AD symptoms. Memantine shields the cells of the brain by blocking the effects of high levels of glutamate. Glutamate is a chemical that assists in the communication between nerve cells which is released in excess when AD damages the nerve cells Frampton, 2014). All these drugs to not completely treat AD but reduces and alleviate the symptoms of the disease.

What is the genetics involved in Alzheimer’s disease?

The Alzheimer’s disease (AD) is a disease of the brain that is irreversible and gradual. The disease is featured by the growth and enlargement of amyloid plaques and neurofibrillary, death of nerve cells and loss of connection between the neurons. There are various evidences proving that there is a link between Alzheimer’s disease and genes on 1, 14, 19, and 21 chromosomes.

So far, researchers have identified four genes that are involved in the etiology of AD. One of the genes includes β-amyloid precursor protein (APP), which is a gene on the 21 chromosomes. APP gene has a critical role in AD pathogenesis. As argued by Sassi et al. (2016) the insoluble neurotoxin derived by APP is triggered by the disproportion between the making of Aβ and sanction which ultimately results in the AD disease. Apolipoprotein E (ApoE), a genetic factor on genetic material 19 is another gene involved in AD. ApoE is found in the plasma and has the role of cholesterol transportation and atherogenic lipoprotein metabolism modulation. As illustrated by Tanzi & Breitner (2000) ApoE is often found among AD patients. The third gene is the presenilin 1, a gene on chromosome 14. Presenilin 1 alterations are the major cause of familial AD. Finally, the Presenilin 2; genetic factor on chromosome 1.Presenilin 2 is a highly homologous presenilin genes whose mutations is a common cause of AD (Mak et al. 2015). Another gene called the αl-antichymotrypsin that on chromosome 14 have been proposed by various researchers to be involved in the Alzheimer’s disease.

References

Frampton, J. (2014). Rivastigmine Transdermal Patch 13.3 mg/24 h: A Review of Its Use in the Management of Mild to Moderate Alzheimer’s Dementia. Drugs & Aging, 31(8), 639-649. doi:10.1007/s40266-014-0197-x

Mak, D. D., Cheung, K., Toglia, P., Foskett, J. K., & Ullah, G. (2015). Analyzing and Quantifying the Gain-of-Function Enhancement of IP3 Receptor Gating by Familial Alzheimer’s Disease-Causing Mutants in Presenilins. Plos Computational Biology, 11(10), 1-22. doi:10.1371/journal.pcbi.1004529

Sassi, C., Ridge, P. G., Nalls, M. A., Gibbs, R., Ding, J., Lupton, M. K., & … Goate, A. M. (2016). Influence of Coding Variability in APP-Aβ Metabolism Genes in Sporadic Alzheimer’s Disease. Plos ONE, 11(6), 1-14. doi:10.1371/journal.pone.0150079

Tanzi, R., & Breitner, J. (2000). Apolipoprotein E genotyping in Alzheimer’s disease. Lancet, 347(9008), 1091.