Question 2 Alzheimer\u2019s dementia (DOCUMENT ATTACHED)
\nwrite https:\/\/monkessays.com
\na.Describe the physiological mechanism by which bexarotene has its potential therapeutic effect in the Alzheimer\u2019s brain, and contrast this mechanism of action to the standard prescribed drug treatments for Alzheimer\u2019s dementia, as discussed in SDK228. (400 words)
\nb.In response to the report, Mary asks: \u201cWhy is the health community not doing more to get these drugs out into the AD population, since the standard drugs used are not effective?\u201d State clearly whether you think this statement about effectiveness is justified and then support your answer with evidence or examples from SDK228. (200 words)
\nc.Write a brief response to Mary in which you explain, using your understanding of information from SDK228 and\/or the report, why Dr Landreth\u2019s finding cannot be translated so quickly into a publically available treatment for Alzheimer\u2019s dementia. You should include at least three separate points in your answer. (200 words)
\nd.The 2016 report from Alzforum details some findings from a human study. How convinced are you by these findings that the effect seen in mice is translatable to humans? Explain your answer. (300 words)<\/p>\n
GUIDANCES:
\nIn this question we are looking to see whether you can draw on a short report to
\ndemonstrate:
\n\u2022 Understanding of theories and evidence concerning the biology of Alzheimer\u2019s dementia
\n(AD), including the role of animal studies
\n\u2022 Understanding of the procedures and challenges involved in clinical trials of drug treatments
\nfor AD
\n\u2022 The capacity to express scientific and clinical findings in an accessible message for a
\nmember of the public
\n\u2022 The capacity to use arguments and evidence to express your own opinion on the potential of
\na drug treatment.
\nYou will need to carefully analyse the provided article and to address theories and evidence
\nconcerning the biology of AD in your answer.
\nTake great care to express all the concepts in your own words, and to include as much specific
\ndetail as the word lengths allow for.
\nQuestion 3 Essay: no more than 1000 words
\n“Can mental health treatments and therapies designed on a \u2018one size fits all\u2019 principle be successful or might it be necessary to consider each individual\u2019s unique combination of biological, psychological and social circumstances?”<\/p>\n
QUIDANCE:
\nTake some time to interpret the question and to make a plan before sitting down to draft your
\nanswer. Highlight the key words in the statement and make a clear argument about the
\nextent to which you agree or disagree with the statement, supporting your answer with a
\nbroad range of module material. Make sure to organise your main points, and the
\nevidence for them into a logical sequence, so that the argument in your essay flows
\nfrom one paragraph to the next.
\nWe are looking to see that you can be evaluative in your answer to the question \u201cCan
\nmental health treatments and therapies designed on a \u2018one size fits all principle\u2019 be
\nsuccessful or might it be necessary to consider each individual\u2019s unique combination
\nof biological, psychological and social circumstances?\u201d
\nMake sure that you include evidence from scientific studies (e.g. experiments, surveys,
\nclinical trials) discussed in the module material. You should also refer to the various personal
\nnarratives and case studies of particular individuals mentioned in SDK228, and represented
\non the multimedia map. However, remember that individual examples provide illustrations of
\nyour arguments rather than scientific evidence as such. You should draw together a broad
\nrange of material from across the module to demonstrate your wide knowledge and your
\nability to integrate this knowledge into an argument. Essays that do not draw across a range
\nof books and the map will lose marks.
\n, https:\/\/monkessays.com, myessyapaper.com<\/p>\n
SDK228 17J EMA Question 2 documents
\nCancer Drug Reverses Symptoms of Alzheimer’s in Mice
\nA drug approved for the treatment of cancer appears to quickly reverse the
\nsymptoms of Alzheimer’s in mice, according to a new study from the US
\npublished in the journal Science on Thursday.
\nThe Food and Drug Administration (FDA) approved bexarotene as a
\ntreatment for cutaneous T cell lymphoma, a type of skin cancer, in 2000. Now
\na team of neuroscientists, led by Dr Gary Landreth, at Case Western Reserve
\nUniversity School of Medicine in Cleveland, Ohio. has shown that when they
\ngave the drug to mice with Alzheimer’s disease, it quickly reversed the
\npathological, cognitive and memory deficits that accompanies it.
\nAbout 5.4 million Americans have Alzheimer’s disease, the most common
\nform of dementia. While the cause of the disease is not well understood,
\nstudies have shown it is linked to an inability to clear away beta-amyloid
\nplaques that accumulate around brain cells.
\nFrom previous work, Landreth had already established that the protein
\nApolipoprotein E (ApoE), the main cholesterol transporter in the brain, also
\nhelps to clear away amyloid beta.
\nSo, he and his colleagues decided to see what effect bexarotene might have
\non this process, since it was already known that one of the effects of the drug
\nis that it stimulates a group of receptors that help control production of ApoE,
\nthe retinoid X receptors (RXR).
\nThey were astonished at the results.
\nWithin six hours of administering bexarotene, levels of soluble amyloid levels
\nfell by 25%. And they were even more impressed when they saw the effect
\nlasted for three days, at which point there was more than 50% reduction in
\namyloid beta plaques. Eventually, the reduction was more than 75%.
\nAnd finally, the change in amyloid levels was accompanied by rapid
\nimprovement in cognitive, social, and olfactory deficits in the three different
\ntypes of mouse model of Alzheimer’s disease.
\nLandreth and colleagues conclude that activating the RXR receptors with
\nbexarotene “stimulates physiological [amyloid beta] clearance mechanisms,
\nresulting in the very rapid reversal of a broad range of [amyloid beta]-induced
\ndeficits”.
\nIn a statement, Landreth described the study, which started as a “far-fetched
\nidea”, as “particularly exciting and rewarding” because they have uncovered
\nnew information and the potential promise of a new treatment for Alzheimer’s
\ndisease. But he added a word of caution:
\n“We need to be clear; the drug works quite well in mouse models of the
\ndisease. Our next objective is to ascertain if it acts similarly in humans. We
\nSDK228 17J EMA Question 2 documents
\nare at an early stage in translating this basic science discovery into a
\ntreatment.\u201d
\nPaddock, C. (2012) \u2018Cancer Drug Reverses Symptoms of Alzheimer\u2019s in Mice\u2019
\nAvailable at https:\/\/www.medicalnewstoday.com\/articles\/241444.php
\n(Accessed 10 November 2017)
\n****************************************************************************************
\nResponse: Why is the public clueless?
\nWhy is the health community not doing more to get these drugs out into the
\nAD population, since the standard drugs used are not effective? These drugs
\nwere also adapted from approved drugs for other conditions, just as
\nbexarotene now used for cancer treatment, is found to be effective for AD.
\nThis is very frustrating to families and patients struggling with the care of and
\nexperience with, Alzheimers. Not to mention the enormous expense for drugs
\nthat give minimal help and the outside medical care that is required.
\nIF THERE IS A DRUG OR PRODUCT OUT THERE THAT SHOWS
\nSIGNIFICANT POSITIVE SAFE RESULTS FOR ANY DISEASE, THE
\nPUBLIC SHOULD BE GIVEN THE INFORMATION QUICKLY AS WELL AS
\nGIVEN THE OPPORTUNITY TO CHOOSE WHETHER OR NOT TO USE IT.
\nposted by Mary on 15 Feb 2012 at 12:31 pm in response to Paddock 2012
\nMary (2012) ‘Response: Why is the public clueless?’, forum message to
\nMedical News Today in response to Paddock 2012, 15th February
\n****************************************************************************************
\nUpdate 2016
\n[A] 68-year-old man, who had an MMSE of 26, was diagnosed with
\nAlzheimer\u2019s based on cognitive testingN. and N.PET scans for A\u03b21
\n. He
\nrequested bexarotene upon learning about Landreth\u2019s mouse study. After
\nconsulting their local ethics committee, his physicians agreed. They
\nprescribed 300mg bexarotene per day, along with 200mg fenofibrate to limit
\nany increase in plasma cholesterol and triglycerides. After six months he
\nunderwent renewed cognitive testing, a second lumbar puncture for fluid
\nbiomarker analysis, and another amyloid PET scan. His memory, as judged
\nby free and cued recall tests, improved by 40 percent and he scored 28 on the
\nMMSE. His CSF2
\n total tau and phospho(rylated)-tau fell by 20 and 10 percent,
\nSDK228 17J EMA Question 2 documents
\nrespectively, while CSF A\u03b2 nudged up by 10 percent. First author Nathalie
\nPierrot and colleagues concluded that the memory and tau effects may be
\nunrelated to amyloid changes, which they considered to be within test-retest
\nvariation.
\n(Alzforum were further told) that the man continued on bexarotene for a total
\nof 23 months. Twenty months after beginning the treatment, his MMSE was
\nonly slightly below his baseline score of 26. Alas, the patient could not afford
\nthe monthly cost of bexarotene\u2014about \u20ac1,200\u2014and stopped taking it. His
\ncognition quickly worsenedN.. MMSE scores at three, five, and eight months
\nafter stopping the drug were 24, 23, and 20, respectively. While there\u2019s no
\nway to tell if this was a placebo effect, (it was) noted that the approved AD
\ndrug galantamine had no effect on his memory when he took it after his initial
\ndiagnosis. \u201cBexarotene is no miracle drug; nevertheless, I think some effect
\nwas present,\u201d lead researcher Ivanoiu told Alzforum. He hopes his findings
\nwill spur further research.
\n1) A\u03b2 is an abbreviation for beta-amyloid
\n2) CSF is an abbreviation for cerebrospinal fluid
\nZakaib, G.T. and Fagan, T. (2016) \u2018Bexarotene- First Clinical Trials highlight
\nContradictions\u2019
\nAvailable at https:\/\/www.alzforum.org\/news\/research-news\/bexarotene-firstclinical-results-highlight-contradictions
\n(Accessed 11 February 2016)<\/p>\n","protected":false},"excerpt":{"rendered":"
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