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Posted: October 20th, 2022
Question 2 Alzheimer’s dementia
Question 2 Alzheimer’s dementia (DOCUMENT ATTACHED)
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a.Describe the physiological mechanism by which bexarotene has its potential therapeutic effect in the Alzheimer’s brain, and contrast this mechanism of action to the standard prescribed drug treatments for Alzheimer’s dementia, as discussed in SDK228. (400 words)
b.In response to the report, Mary asks: “Why is the health community not doing more to get these drugs out into the AD population, since the standard drugs used are not effective?” State clearly whether you think this statement about effectiveness is justified and then support your answer with evidence or examples from SDK228. (200 words)
c.Write a brief response to Mary in which you explain, using your understanding of information from SDK228 and/or the report, why Dr Landreth’s finding cannot be translated so quickly into a publically available treatment for Alzheimer’s dementia. You should include at least three separate points in your answer. (200 words)
d.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)
GUIDANCES:
In this question we are looking to see whether you can draw on a short report to
demonstrate:
• Understanding of theories and evidence concerning the biology of Alzheimer’s dementia
(AD), including the role of animal studies
• Understanding of the procedures and challenges involved in clinical trials of drug treatments
for AD
• The capacity to express scientific and clinical findings in an accessible message for a
member of the public
• The capacity to use arguments and evidence to express your own opinion on the potential of
a drug treatment.
You will need to carefully analyse the provided article and to address theories and evidence
concerning the biology of AD in your answer.
Take great care to express all the concepts in your own words, and to include as much specific
detail as the word lengths allow for.
Question 3 Essay: no more than 1000 words
“Can mental health treatments and therapies designed on a ‘one size fits all’ principle be successful or might it be necessary to consider each individual’s unique combination of biological, psychological and social circumstances?”
QUIDANCE:
Take some time to interpret the question and to make a plan before sitting down to draft your
answer. Highlight the key words in the statement and make a clear argument about the
extent to which you agree or disagree with the statement, supporting your answer with a
broad range of module material. Make sure to organise your main points, and the
evidence for them into a logical sequence, so that the argument in your essay flows
from one paragraph to the next.
We are looking to see that you can be evaluative in your answer to the question “Can
mental health treatments and therapies designed on a ‘one size fits all principle’ be
successful or might it be necessary to consider each individual’s unique combination
of biological, psychological and social circumstances?”
Make sure that you include evidence from scientific studies (e.g. experiments, surveys,
clinical trials) discussed in the module material. You should also refer to the various personal
narratives and case studies of particular individuals mentioned in SDK228, and represented
on the multimedia map. However, remember that individual examples provide illustrations of
your arguments rather than scientific evidence as such. You should draw together a broad
range of material from across the module to demonstrate your wide knowledge and your
ability to integrate this knowledge into an argument. Essays that do not draw across a range
of books and the map will lose marks.
, https://monkessays.com, myessyapaper.com
SDK228 17J EMA Question 2 documents
Cancer Drug Reverses Symptoms of Alzheimer’s in Mice
A drug approved for the treatment of cancer appears to quickly reverse the
symptoms of Alzheimer’s in mice, according to a new study from the US
published in the journal Science on Thursday.
The Food and Drug Administration (FDA) approved bexarotene as a
treatment for cutaneous T cell lymphoma, a type of skin cancer, in 2000. Now
a team of neuroscientists, led by Dr Gary Landreth, at Case Western Reserve
University School of Medicine in Cleveland, Ohio. has shown that when they
gave the drug to mice with Alzheimer’s disease, it quickly reversed the
pathological, cognitive and memory deficits that accompanies it.
About 5.4 million Americans have Alzheimer’s disease, the most common
form of dementia. While the cause of the disease is not well understood,
studies have shown it is linked to an inability to clear away beta-amyloid
plaques that accumulate around brain cells.
From previous work, Landreth had already established that the protein
Apolipoprotein E (ApoE), the main cholesterol transporter in the brain, also
helps to clear away amyloid beta.
So, he and his colleagues decided to see what effect bexarotene might have
on this process, since it was already known that one of the effects of the drug
is that it stimulates a group of receptors that help control production of ApoE,
the retinoid X receptors (RXR).
They were astonished at the results.
Within six hours of administering bexarotene, levels of soluble amyloid levels
fell by 25%. And they were even more impressed when they saw the effect
lasted for three days, at which point there was more than 50% reduction in
amyloid beta plaques. Eventually, the reduction was more than 75%.
And finally, the change in amyloid levels was accompanied by rapid
improvement in cognitive, social, and olfactory deficits in the three different
types of mouse model of Alzheimer’s disease.
Landreth and colleagues conclude that activating the RXR receptors with
bexarotene “stimulates physiological [amyloid beta] clearance mechanisms,
resulting in the very rapid reversal of a broad range of [amyloid beta]-induced
deficits”.
In a statement, Landreth described the study, which started as a “far-fetched
idea”, as “particularly exciting and rewarding” because they have uncovered
new information and the potential promise of a new treatment for Alzheimer’s
disease. But he added a word of caution:
“We need to be clear; the drug works quite well in mouse models of the
disease. Our next objective is to ascertain if it acts similarly in humans. We
SDK228 17J EMA Question 2 documents
are at an early stage in translating this basic science discovery into a
treatment.”
Paddock, C. (2012) ‘Cancer Drug Reverses Symptoms of Alzheimer’s in Mice’
Available at https://www.medicalnewstoday.com/articles/241444.php
(Accessed 10 November 2017)
****************************************************************************************
Response: Why is the public clueless?
Why is the health community not doing more to get these drugs out into the
AD population, since the standard drugs used are not effective? These drugs
were also adapted from approved drugs for other conditions, just as
bexarotene now used for cancer treatment, is found to be effective for AD.
This is very frustrating to families and patients struggling with the care of and
experience with, Alzheimers. Not to mention the enormous expense for drugs
that give minimal help and the outside medical care that is required.
IF THERE IS A DRUG OR PRODUCT OUT THERE THAT SHOWS
SIGNIFICANT POSITIVE SAFE RESULTS FOR ANY DISEASE, THE
PUBLIC SHOULD BE GIVEN THE INFORMATION QUICKLY AS WELL AS
GIVEN THE OPPORTUNITY TO CHOOSE WHETHER OR NOT TO USE IT.
posted by Mary on 15 Feb 2012 at 12:31 pm in response to Paddock 2012
Mary (2012) ‘Response: Why is the public clueless?’, forum message to
Medical News Today in response to Paddock 2012, 15th February
****************************************************************************************
Update 2016
[A] 68-year-old man, who had an MMSE of 26, was diagnosed with
Alzheimer’s based on cognitive testingN. and N.PET scans for Aβ1
. He
requested bexarotene upon learning about Landreth’s mouse study. After
consulting their local ethics committee, his physicians agreed. They
prescribed 300mg bexarotene per day, along with 200mg fenofibrate to limit
any increase in plasma cholesterol and triglycerides. After six months he
underwent renewed cognitive testing, a second lumbar puncture for fluid
biomarker analysis, and another amyloid PET scan. His memory, as judged
by free and cued recall tests, improved by 40 percent and he scored 28 on the
MMSE. His CSF2
total tau and phospho(rylated)-tau fell by 20 and 10 percent,
SDK228 17J EMA Question 2 documents
respectively, while CSF Aβ nudged up by 10 percent. First author Nathalie
Pierrot and colleagues concluded that the memory and tau effects may be
unrelated to amyloid changes, which they considered to be within test-retest
variation.
(Alzforum were further told) that the man continued on bexarotene for a total
of 23 months. Twenty months after beginning the treatment, his MMSE was
only slightly below his baseline score of 26. Alas, the patient could not afford
the monthly cost of bexarotene—about €1,200—and stopped taking it. His
cognition quickly worsenedN.. MMSE scores at three, five, and eight months
after stopping the drug were 24, 23, and 20, respectively. While there’s no
way to tell if this was a placebo effect, (it was) noted that the approved AD
drug galantamine had no effect on his memory when he took it after his initial
diagnosis. “Bexarotene is no miracle drug; nevertheless, I think some effect
was present,” lead researcher Ivanoiu told Alzforum. He hopes his findings
will spur further research.
1) Aβ is an abbreviation for beta-amyloid
2) CSF is an abbreviation for cerebrospinal fluid
Zakaib, G.T. and Fagan, T. (2016) ‘Bexarotene- First Clinical Trials highlight
Contradictions’
Available at https://www.alzforum.org/news/research-news/bexarotene-firstclinical-results-highlight-contradictions
(Accessed 11 February 2016)
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