Get help now
  • Pages 5
  • Words 1096
  • Views 370
  • Download


    Verified writer
    • rating star
    • rating star
    • rating star
    • rating star
    • rating star
    • 5/5
    Delivery result 2 hours
    Customers reviews 339
    Hire Writer
    +123 relevant experts are online

    Alzheimer’s D isease Essay (1096 words)

    Academic anxiety?

    Get original paper in 3 hours and nail the task

    Get help now

    124 experts online

    Alzheimer’sDisease Darina Vrublevskaya Mrs. Orlovsky SBI 3U1 Tuesday, April 18, 2017 Introduction Alzheimer’s disease is completelyirreversible, affecting nerve cells of the brain and leading to severe memory impairment and progressive loss of mental abilitiesin elderly(Encyclopedia Britannica, 2017). The disease most commonly affects those after the age of 65, but can still be diagnosed earlier.

    There is an estimated 26 millionpeople worldwide living with the condition today, making it a threat to public health since the populations are tremendously rising (Cruchaga, et al,2014, vol. (17)9 1138+). By age 85, it is expected that half of all people will have Alzheimer’s (Hoyle, 2014). Alzheimer’s is the most common form of dementia. Dementia is a variety of symptoms including memory loss, confusion, difficulties communicating, reasoning, and coordinating. Thedisease got so serious, thattotal cost of dementia is $818 million (USD) and is expected to reach $1 trillion (USD) by 2018 (Liv, et al, 2017, vol.

    (6) 1). The name of the disease comes from Dr. Alois Alzheimer who waspsychiatrist and a neuropathologistthatdiscovered the disease in 1907(Alzheimer Society Canada, 2016). Alois studied one of his patients whosepersonality and mental abilities were obviously detoriating; sheforgot things, became paranoid, and acted strangely(World of Genetics,Gale,2013).

    His researchrevealed two types of lesionsafterobserving parts of her brain through a microscope. Aloisfound senileplaques,which areabnormalclusters of protein fragments thatbuild up between nerve cells. He also discovered neurofibrillary tanglesthatdestroy a vital cell transport system made of proteins. Etiology There are various different ways to detect Alzheimer’s disease.

    In fact, victims tend to have shrunken brains which affect the brains function. This shrinkage occurs due to loss of brain cells. In order to detect the disease, there are blood tests that measure increased proteinamounts in certain white blood cells and also tomography that detects levels of enzyme in cerebrospinal fluid (Encyclopedia Britannica, 2017). The spinal fluid is found to predict Alzheimer disease development in persons with early loss of memory and confirm existing Alzheimer disease in persons who already hadsymptoms of the disease (World of Genetics,Gale,2016). There are two ways a person can get the disease, through a family member or due to environmental factors.

    Familial Alzheimer’s is extremely rare and entirely inherited, as the genes are mutatedthatdevelopabnormal characteristics (Liv, et al, 2017). Achild whose parent has Alzheimer’s has a half chance of inheriting the disease-causing gene (Friedman,et al,2016). Sporadic Alzheimer’s disease isthemost commonof receiving the disease. Ithas no specific family link since it develops due tothe environmentand lifestyle(Cruchaga,et al,2014, vol. 17(9) 1138+).

    Familial Alzheimer’s cannot be prevented because it runs in one’s genes. However, sporadic Alzheimer’s can possibly be prevented if a healthy lifestyle is maintained. It’s important that those who are young take care of themselves until old age, in order to reduce the risk of developing Alzheimer’s or any other disease. There are three types of stages of the disease:theearly stage,themiddle stage, and the late stagein Alzheimer’s disease.

    The early stage includes mild impairment due to symptoms such as forgetfulness, communication difficulties, and changes in mood and behavior (Alzheimer Society Canada, 2016). The individuals who are in themiddle stage,battle with intuition related and usefulcapacities and require help many tasks(Gilmour, et al, 2016,27(5), 11+). The late stage is known as theseverestage;when anindividual might be not abletakecare forthem,and really requireconstant supervision and help (Bali, et al, 2010,13(6), 89). Alzheimer’s develops in the brain. Before the appearance of the symptoms, senile plaques and neurofibrillary tangles form in the brain. The brain is made up of neurons that are interconnected to form a vast network.

    These connections, known as synapses enable the transmission of information from one neuron to another. Senile plaques are composed of amyloid betaprotein and neurofibrillary tangles are composed of tauprotein (Friedman,et al,2016). The senile plaque is formedon the surface of the neuronwherelarge proteinfreestheamyloid beta. Amyloid beta is then cleared in the body.

    In Alzheimer’s, there is imbalance as the beta protein is no longer regulated and is found in a greaterquantity(Bali,et al,2010,13(6), 89). The amyloid beta then assembles to form senile plaques. Senile plaques are found in the cortex of the brain in the hippocampus and then reach the whole brain, surrounding nerve cells in the part of the brain that allows access to emotions and mood(Ledford, 2011,469(7331),458). Neurofibrillarytangles are formed when a neuron communicates with another. When it does, a signal travels within the body known as soma, to the synapse to transferinformation (Gilmour, 2016, 27(5), 11+).

    The signal passesthrough the neuron composed of microtubules. These microtubulesare normal tau protein. In Alzheimer’s, they become defective, and the neuron collapses and the connection between neurons are lost (Friedman. 2016). The two lesions spreadthroughoutthe brain.

    However, neurofibrillary tangles and senile plaques do not follow the same pathway. Neurofibrillarytangles first develop in the region called hippocampus which is essential to memory and learning (World of Genetics,Gale,2013). They then reach the whole brain, and theprocesscorresponds with the symptoms of the disease. Conclusion Alzheimer’sdisease is a devastating condition, currently without an effective cure, treatment or preventions that robs people from their memories and abilities(Cruchaga,et al,2014, vol. (17)9 1138+). Emotions and mood is strongly impacted and individuals may lose interest in activities they use to enjoy, as well as become less expressive to those around them (Alzheimer Society Canada, 2016).

    Currently,the cause of the disease is not quite exactly known, but there are many different believable supporting theories behind the cause. It’s saddening how loved ones do not get a chance to say goodbyebefore one’s memory is lost. Millions of families grieve due to the Works Cited Alzheimer disease. (2017). In Encyclopedia Britannica.

    Retrieved from http://school. eb. com/ Alzheimer Society Canada. (2017). Find Alzheimer Societies in Canada.

    Retrieved from http://www. alzheimer. ca/ Bali, J. , Halima, S. , Felmy, B.

    , Goodger, Z. , Zurbriggen, S. , ; Rajendran, L. (2010). Cellular basis of Alzheimer’s disease. Annals of Indian Academy of Neurology,13(6), 89.

    Retrieved fromhttp://go. galegroup. com/ Hao, W. , ; Friedman, A. (2016). Mathematical model on Alzheimer’s disease.

    BMC Systems Biology,10(1). Retrieved fromhttp://link. galegroup. com/ Hoyle, B. (January 15, 2014). Alzheimer’s disease,The Gale Encyclopedia of Science (5th ed.

    ). Retrieved fromhttp://link. galegroup. com/ Ledford, H.

    (January 27, 2011). Alzheimer’sdisease probe nears approval: imaging technique could help to resolve questions about brain plaques associated with the condition. Nature,469(7331), 458. Retrieved fromhttp://link. galegroup.

    com/ Lord. , J ; Cruchaga. , C. (September, 2014).

    The epigenetic landscape of Alzheimer’s disease. Nature Neuroscience,17(9) 1138+. Retrieved fromhttp://link. galegroup.

    com/ Wong,L. ,Gilmour, H. , ; Ramage-Morin,L. (2016). Alzheimer’s disease and other dementias in Canada. Health Reports,27(5), 11+.

    Retrieved from http://link. galegroup. com/ Xiao, T. , Zhang, W.

    , Pan, C. , Liv, X. , ; Shen, L. (February 2, 2017). The role of exosomes in the pathogenesis of Alzheimer’s disease.

    Translocational Neurogeneration,(6) 1. Retrieved fromhttp://www. researchgate. net World of Genetics, Gale, Science in Context,2013. Alzheimer Disease.

    Retrieved from

    This essay was written by a fellow student. You may use it as a guide or sample for writing your own paper, but remember to cite it correctly. Don’t submit it as your own as it will be considered plagiarism.

    Need custom essay sample written special for your assignment?

    Choose skilled expert on your subject and get original paper with free plagiarism report

    Order custom paper Without paying upfront

    Alzheimer’s D isease Essay (1096 words). (2018, Dec 29). Retrieved from

    We use cookies to give you the best experience possible. By continuing we’ll assume you’re on board with our cookie policy

    Hi, my name is Amy 👋

    In case you can't find a relevant example, our professional writers are ready to help you write a unique paper. Just talk to our smart assistant Amy and she'll connect you with the best match.

    Get help with your paper