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Alzheimer Disease: The Untouchable Presenile Dementia

Info: 2241 words (9 pages) Nursing Assignment
Published: 20th Aug 2020

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Tagged: dementiadiseasealzheimers

One of the most accelerating neurological disorder among the elderly population, Alzheimer disease serves as the common cause for presenile dementia hitting the number of 13.8 million by 2050. (Herbert L.E, et.al).  With increasing in ageing population the neurodegenerative disease rises while enhanced and magnified research has been conducted but no productive answer has been out yet (Cavanough 1). The aim of this research is to discuss some of the topics which leads to Alzheimer Disease such as deficiency of Vitamin D and accumulation of amyloid-beta in the brain and the approaches which has been taking place over years using animal models such as transgenic or inbred mice in order to epitomize the genetical traits on human beings to cure it on a biochemical and genetic level.

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Certain changes occur when the body is deficient of components that are needed to the brain, bones following the spinal cord and the rest of the body.  The deficiency of Vitamin D in elderly masses is observed higher in number compared to young people and one of the reason is to less exposure to the sun (Gargland 1). Vitamin D being a secosteroid hormone, is an endocrine mechanism which is known to control calcium and phosphorus homeostasis helps in controlling the Ca2+ via the voltage-gated calcium channels which are used by the brain of the human body to function.(Dursun, et.al 1).  In 1992, Sutherland researched regarding the role of vitamin D contributing to Alzheimers Disease which delivered a hypothesis that a perpetual deficiency of vitamin D receptor (VDR) can lead to disturbance in the calcium homeostasis in the brain via neurons (Southerland, et.al) (Dursun, et.al).  As reported by Dr. Dursun and Dr. Duryug in their journal called “The Effects of Vitamin D Receptor Silencing on the Expression of LVSCC-A1C and LVSCC-A1D and the Release of NGF in Cortical Neurons” the Third National Health and Nutrition Examination Survey (USA), vitamin D regulated 1000 genes at different stages of development which when unregulated effects wide-spectrum of  masses focusing more on elderly generation. (Duyug, Dursun 1), (Cekic, et.al). A previous study on hippocampal neurons by Dr. Brewer using the rat hippocampal cultures were treated for days with vitamin D hormone which comes out that vitamin D regulates calcium homeostasis by lowering the level of L- type voltage-sensitive calcium channels (LVSCC) located in the neurons including it regulates the nerve growth factor expression. (Brewer 98-108).

Regardless the deficiency of Vitamin D approaching AD, a recent journal states that an uncontrolled assembly of amyloid-beta peptide in the brain could be a cause for the birth of Alzheimer Disease which can cause alteration in the physiology of the brain over a certain period of years. Neurons and platelets release a peptide called amyloid-Beta which is acquired from Amyloid precursor protein (Kucheryavykh 1). Amyloid-beta 42 and Amyloid-beta 40 were the first amyloids known to be concerned in the process of Alzheimer disease maturation (Helmen 2). Victims suffering from the mild cognitive disorder which also includes Parkinson’s disease have shown lower levels of Amyloid-beta 42 in the cerebrospinal fluid which could be one of the indications for early detection of Alzheimer disease (Palmqvist 2). As Dr. Nalinaeva mentioned in her article among other researchers in the journal called “Amyloid-clearing proteins and their epigenetic regulation as a therapeutic target in Alzheimer’s disease” that the accumulation of Amyloid–beta could cause-effect of the normal diet, hypoxia, brain trauma and mutation in genes which could affect both the deposit of Amyloid-Beta and the proteolytic cleavage of proteins (Nalivaeva 1). As mentioned before, hypoxia is one of the symptoms of the accumulation of amyloid-beta in the brain, this could be due to an impairment in the production of ATP in the mitochondria. A study on transgenic mice has shown that the secretion of amyloid-Beta in the mitochondrial matrix leads to the expression of Amyloid precursor protein in the brain which lowers the respiratory chain activity (Xi, et.al 1). Considering all the hypothesis, there is various impairment of mitochondrial function which raises the thoughts on Alzheimer disease. Although, taking all the evidence and concern together it cannot be said that mitochondrial disorder is an ultimate cause of Alzheimer disease. Huntington’s disease, amyotrophic lateral sclerosis are diseases which have seen to occur in patients having a mitochondrial impairment (Guo X, et.al).

Disregarding the fact of new experiments and advancement towards the neurology of Alzheimer disease, it still symbolizes a divergent and exceptional disease in its physiology, treatment and the most important the feedback to the treatment (Husain 1). The unnatural behaviour and high level of complexity of Alzheimer Disease have been visible after the result of drug development pipeline 2019. As the population of ageing people increase the risk of mild cognitive disease increase which increases of patients suffering from neurodegenerative disease. “There have been no new drugs approved since 2003, and there are no approved disease modifying treatments (DMTs) for AD” (Cummings et.al), this statement by the Drug Development of Alzheimer Disease 2019 turns out to be a fact of threat for the upcoming ageing generation. (Cummings, et.al). Animal models, specifically mouse and rat models sharing almost identical genes as human beings are being used for the approval of drugs. Flipping the coin on the other side, there are assumptions and different outlooks regarding the translation of animal-to-human notions which has been completely misguided including the fact that due to biological limitation a single model is not suitable to show all the characters and aspects of Alzheimer disease (Pound 1). These models could be used during the early stage of Alzheimer because these models lack the regenerative neurons. Certain researches have shown that zebrafish could be one of the candidates used to study neurogenesis which is regeneration to replace old neutrons (Kizil 1).  Neurogenesis is one of the approaches were the old neutrons are replaced by new neutrons and it could be one step to ameliorate the condition of Alzheimer, being a challenging step because some researchers believe that it may affect the amyloid secretion on the stem cells of the human brain (Bhattrai 1). Here, a question arises: can Alzheimer disease be treated thorough neurodegeneration? No doubt, the brain of zebrafish and human are quite different, but according to Kizil et.al the brain of zebrafish responded to neurodegeneration by using neuro-inflammatory and increase in proliferation and reduced in neural cell plasticity (Kizil 1). There are several negative results of drug development using an animal model, they have been a huge success in oncology (Perlman,1). According to Gonzalves, there are only five drugs approved by the FDA for Alzheimer disease, different approaches were under clinical trial for the stimulation of the brain using electrical current and laser therapy but the majority of them end up effectuating mitochondrial dysfunction, inflammation and amyloid-beta (Gonzalves, et.al 1).

Alzheimer disease has been one of the challenges for the researchers, physician and individual to the population level. Public health-based researchers are still identifying the neuropathological changes and cognitive impairment caused by Alzheimer disease: more observational and standardize therapautic experiment should be taking place. Despite the fact that dementia or AD are also affected by age and gender, these two factors should not be out of sight. Clarification regarding the relationship between neuropathology and different perception and jurisdication regarding AD could be one of the steps to approach the targeting factors causing dementia.

Works Cited

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2. Cavanaugh, S., J. Pippin, and N. Barnard. “Animal Models of Alzheimer Disease: Historical Pitfalls and a Path Forward”. ALTEX – Alternatives to Animal Experimentation, Vol. 31, no. 3, Aug. 2014, pp. 279-02, doi:10.14573/altex.1310071.

3. Garland, Cedric F et al. “The role of vitamin D in cancer prevention.” American journal of public health vol. 96,2 (2006): 252-61. doi:10.2105/AJPH.2004.045260

4. Sutherland MK, Somerville MJ, Yoong LK, Bergeron C, Haussler MR, McLachlan DR (1992) Reduction of vitamin D hormone re- ceptor mRNA levels in Alzheimer as compared to Huntington hip- pocampus: correlation with calbindin-28k mRNA levels. Brain Res Mol Brain Res 13:239–250

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6. Brewer LD, Thibault V, Chen KC, Langub MC, Landfield PW, et al. (2001) Vitamin D hormone confers neuroprotection in parallel with downregulation of L-type calcium channel expression in hippocampal neurons. J Neurosci 21: 98–108.

7. Zhenbo Chen, Shanwei Tao, Xiaohui Li, Xudong Zeng, Mirong Zhang & Qinghe Yao “Anagliptin protects neuronal cells against endogenous amyloid β (Aβ)-induced cytotoxicity and apoptosis, Artificial Cells”. Nanomedicine and Biotechnology,  Volume 47:1, pp. 2213-2220, 2019 DOI: 10.1080/21691401.2019.1609979  https://doi.org/10.1080/21691401.2019.1609979

8. Kucheryavykh, Lilia Y et al. “Amyloid Beta Peptide Is Released during Thrombosis in the Skin.” International journal of molecular sciences vol. 19,6 1705. 8 Jun. 2018, doi:10.3390/ijms1906170

9. Helman, Alex M et al. “Microbleeds and Cerebral Amyloid Angiopathy in the Brains of People with Down Syndrome with Alzheimer’s Disease.” Journal of Alzheimer’s disease : JAD vol. 67,1 (2019): 103-112. doi:10.3233/JAD-180589.

10. Palmqvist, Sebastian et al. “Cerebrospinal fluid analysis detects cerebral amyloid-β accumulation earlier than positron emission tomography.” Brain : a journal of neurology vol. 139,Pt 4 (2016): 1226-36. doi:10.1093/brain/aww015

11.  Nalivaeva, Natalia N et al. “Amyloid-clearing proteins and their epigenetic regulation as a therapeutic target in Alzheimer’s disease.” Frontiers in aging neuroscience vol. 6 235. 17 Sep. 2014, doi:10.3389/fnagi.2014.00235

12. Xi Chen, David Stern and Shi Du Yan, “ Mitochondrial Dysfunction and Alzheimers Disease”, Current Alzheimer Research (2006) 3: 515. https://doi.org/10.2174/156720506779025215

13. Guo X, Sun X, Hu D, et al. “VCP recruitment to mitochondria causes mitophagy impairment and neurodegeneration in models of Huntington’s disease”. Nat Commun. 2016;7:12646. Published 2016 Aug 26. doi:10.1038/ncomms12646.

15. Masud Husain, “Alzheimer’s disease: time to focus on the brain, not just molecules”. Brain, Volume 140, Issue 2, February 2017, pp. 251–253. https://doi.org/10.1093/brain/aww353

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