Tentative Link of Brain Trauma and Neurodegenerative Disease

As most of us know, tonight is the annual rivalry football game between the Arizona State Sun Devils and the Arizona Wildcats.  In addition to our very intense rivalry game, there are tons of significant rivalry games across the US today.  That being said, there's always a lot of clammer leading up to a rivalry game including phrases from team to team that hint at wanting to "kill" the opponent or at least "knock their heads off their shoulders".  All of this rivalry talk got me thinking about the significance of head injuries to neurodegenerative diseases.  The findings were not too surprising:

I came across a Cambridge University study that inadvertently focused on the significance of brain injury and Alzheimer's that was published just two weeks ago!  The researchers used a very simple cultured-cell model to examine the activity of a specific protein called Tubulin Associated Protein Unit (Tau).  They noted that many post-death brain examinations of Alzheimer's patients yield the discovery of high amounts of abnormally-clumped Tau protein throughout the brain.  The researchers introduced the Tau protein to the cell culture (raised to behave like brain and nervous cells) and observed a new phenomenon.  They saw that when Tau is introduced to the outside of the cells, they immediately begin to endocytose the extracellular Tau protein.  As the protein was endocytosed it clumped very quickly inside of the cells; they very significantly noted that Tau already in the cell before endocytosis also began to clump abnormally even if it did not come into contact with the extracellular Tau.

The researchers go on to note that in the human model, they would expect Tau escaping from brain tissues to leak and cause similar behavior.  They note that one very likely method for Tau to leak comes from damage incurred from significant head trauma.  The researchers do, however, admit that this is a very preliminary model and that they will use it to evolve future studies.  They will focus on the source of extracellular Tau and where it meets normal Tau as it is endocytosed.

Now I'm really rootin' for a Wildcats' victory today, but after reading this, I can honestly say that I hope for no Sun Devil's head to be knocked from their shoulders.  It will be interesting to see new studies emerging from these preliminary findings, perhaps a study including American football players (or other contact sports) and their prevalence of Alzheimer's Disease.

Go 'Cats!

Sources:
-Medical News Today:  http://www.medicalnewstoday.com/articles/269460.php
-Cambridge Press Release:  http://www.cam.ac.uk/research/news/protein-released-from-cells-triggers-chain-reactions-that-could-cause-alzheimers-disease
--The published study:  http://www.jbc.org/content/early/2013/11/14/jbc.M113.515445.full.pdf

Meditation Aids in Slowing of Progression of Alzheimer's?

Meditation is known to cause changes in the brain, but the effects of those changes have not been thoroughly studied. Researchers collected data from 14 individuals ages 55-90 that had been diagnosed with mild cognitive impairment, a stage typically before progression to Alzheimer's disease. The participants were randomly placed in two different groups: one that participated in Mindfulness-Based Stress Reduction (MBSR) and another that did not. MBSR is a combination of meditation and yoga. The participants in the MBSR group met for 2 hours each week to participate in the activity for eight weeks.

In order to study the effects of meditation on the brain, researchers compared functional MRI (fMRI) images from baseline and then after eight weeks for both groups. The results of the fMRI images showed that the group that participated in MBSR had significantly improved functional connectivity in the areas of the default mode network. The default mode network is the part of the brain that is engaged when remembering past events or envisioning the future, typically connectivity decreases in this part of the brain during the pathophysiology of Alzheimer's disease. They also found that both groups experienced atrophy in the hippocampus, as expected, but those that had practiced MBSR experienced less atrophy.

I like this study because I feel like meditation or MBSR are manageable activities for senior citizens. I think it could also be easy for assisted living or senior centers to incorporate classes that enable seniors to participate in these activities. Additionally, it is not a large time commitment. While the results of this study are promising, I do think that more research is needed on this topic to further examine if MBSR has long term cognitive benefits for Alzheimer’s disease because the researchers did not directly test cognitive function and this study only had a small sample with 14 participants.

Sources:

Lawman, Kelly. "Stress Reduction through Meditation May Aid in Slowing the Progression of Alzheimer's Disease." Beth Israel Deaconess Medical Center, 19 Nov. 2013. Web. 27 Nov. 2013. <http://www.bidmc.org/News/In-Research/2013/November/Wells-Meditation.aspx>.

Stem cells delay disease onset in mice with neurodegenerative disease!

Stem cells delay disease onset in mice with neurodegenerative disease

As soon as I saw this title I thought this would be something cool to read and share! Stem cell research, as we know, is a very interesting and young field. This article is talking about how stem cells have helped detoxify poisoned brains of rats for a period of time. This paper is talking about a neurodegenerative disease called Infantile Neural Ceroid Lipofuscinosis (Batten Disease). In this disease the brain cells lack the enzymes needed to get rid of the byproducts made by the cells causing toxicity in the brain. This disease causes seizures, cognitive and motor decline, blindness and early death.

Palo Alto, California-based company StemCells Inc. is running trials to find if stem cell therapy will help this disease. The idea behind these trials is that the transplanted cells will secrete the missing enzymes, which will improve the health of the patients. Another research was done earlier by another company for treating a different disease similar to Batten disease by stem cells and this study showed improvement to the life span of the rats tested on.

The major thing they tested for in this research was the toxin, lipofucin, which builds up in the patients brain and cause the toxicity. After the mice received the transplant they showed much improvement in health: a 37% decrease of toxin in their cortex and 50% decrease of toxin in their hippocampus.

The most interesting aspect of this article, in my opinion, was the improvements seen from the stem cell therapy. It is important to remember that this is an animal model which could very well not work on human subjects. It is amazing that science has come so far, that we are finding cures to diseases that could potentially be beneficial to humans. Nonetheless stem cell research (or Cures for Batten’s disease) is a field of research, which in my opinion, should be looked into much more than it currently is!

 

The link:

http://www.nature.com/stemcells/2009/0909/090910/full/stemcells.2009.119.html

 

Baker, Monya. "Stem cells delay disease onset in mice with neurodegenerative disease." Nature Reports Stem Cells. (September, 2009): n. page. Web. 27 Nov. 2013. <http://www.nature.com/stemcells/2009/0909/090910/full/stemcells.2009.119.html>.

CSF Inflammatory Markers in PD and Non-Motor Symptoms

When I think about Parkinson's disease the first symptoms that come to my mind are the motor skill symptoms like trembling, stiffness, and impaired balance. However, there are also non-motor symptoms like depression, fatigue, and cognitive impairment that many people with Parkinson's disease are affected by. Previous research has linked brain inflammation in Parkinson's to these non-motor symptoms. However, in a recent study published in Brain, Behavior, and Immunity researchers studied the correlation between cerebrospinal fluid (CSF) inflammatory markers and non-motor symptoms.

For the study, there were 87 people with Parkinson's disease and 37 healthy individuals as the control group. They measured the amount of C-reactive protein, IL-6, eotaxin, TNF-alpha, IP-10, MCP-1, and MIP-1beta extracted from lumbar 3 (L3) to sacral 1 (S1) using a multiplex electrochemiluminescence based immunoassay.

In analyzing the data they found that an increased amount of inflammatory markers was significantly associated with more severe symptoms of depression, fatigue, anxiety, and cognition in the Parkinson's disease group. After excluding factors that may have influenced the results like length of time with Parkinson's disease, gender, age, somatic illness, and dementia,  high CRP levels were significantly associated with severe symptoms of depression and fatigue. Additionally, high levels of MCP-1 were significantly associated with more severe depression symptoms.

I found this study interesting as I previously had limited knowledge about Parkinson's disease. If the findings in this study are supported by other research, this could lead to anti-inflammatory medications being used for the treatment of non-motor symptoms of Parkinson's disease.

Sources:
Lindqvist, D., Hall, S., Surova, Y., Nielsen, H., Janelidze, S., Brundin, L., & Hansson, O. (2013). Cerebrospinal fluid inflammatory markers in Parkinon's disease -- Associations with depression, fatigue, and cognitive impairement. Brain, Behavior, and Immunity, 33, 183-189.

Brain imaging differences in infants at genetic risk for Alzheimer's

APOE-E4 is a gene that is present in about 25% of the U.S. population. Although not everyone who has the gene gets Alzheimer’s, 60% of Alzheimer’s patients have at least one copy of this gene (2). The gene is thought to have several different roles in the brain and blood. The APOE proteins are the main transporters of lipids in the brain; however, APOE-E4 is not as efficient at lipid and A-beta transportation as other variants of this gene. Therefore, the brain is more vulnerable to acute injuries and the stresses of aging (1).

In a recent study researchers from Brown University and Banner Alzheimer’s Institute have found that infants who carry the APOE-E4 gene tend to have differences in brain development in comparison to infants without the gene. The researchers used a specialized MRI technique to image the brain of 162 infants between 2 months and 25 months, 60 of which had the E4 variant of the APOE gene. In comparing the MRI images, the researchers found that the children with APOE-E4 gene tend to have increased brain growth in the frontal lobe and decreased growth in several parts in the middle and rear of the brain. The areas of decreased growth are the same areas that tend to be affected by Alzheimer’s disease (2).

It is important to recognize that these findings do not mean that the infants with this variant are “destined” to develop Alzheimer’s, but that those who carry the gene APOE-E4 tend to develop differently from a young age. The researchers postulated that these changes in development may provide a foothold for the pathology of Alzheimer’s to occur (2).

While this study does not allow for the early diagnosis of Alzheimer’s or a new ‘miracle’ treatment option, I think the results will be extremely beneficial in the study of Alzheimer’s disease and how the E4 variant contributes to risk of the disease later in life.

Sources:

1. Schnabel, Jim. "Why Does APOE-E4 Make Alzheimer's More Likely?" The Dana Foundation. N.p., 07 July 2011. Web. 26 Nov. 2013. <http://www.dana.org/news/features/detail.aspx?id=33588>.

2. Stacey, Kevin. "Brain Imaging Differences in Infants at Genetic Risk for Alzheimer's." Brain Imaging Differences in Infants at Genetic Risk for Alzheimer's. EurekAlert, 25 Nov. 2013. Web. 26 Nov. 2013. <http://www.eurekalert.org/pub_releases/2013-11/bu-bid112213.php>.

More on Multiple Sclerosis

More On Multiple Sclerosis

During the last two weeks we have discussed multiple sclerosis as a neurodegenerative disease, but we have not discussed in detail that there are four different types of multiple sclerosis.

Primary Progressive Multiple Sclerosis:

In this subgroup, the symptoms of the patient continually progress after diagnosis. Unlike the other MS subgroups, there are equal proportions of men and women with Primary Progressive, whereas in the other subgroups women outnumber men 3 to 1. Additionally, patients are usually diagnosed at an older age (the average age being 40). Another unique and frustrating characteristic of this group is that treatments have not been as effective for these patients.

Relapse-Remitting Multiple Sclerosis:

This is the most common type with 85% of MS patients displaying Relapse-Remitting MS. As the name suggests the unique and uniting characteristic of this subgroup is that patients suffer periodic attacks (relapses) and then go through periods of remission. The length of relapse, severity of relapse, and the pattern of nerves affected vary depending on the person. Over time, generally 10-20 years, people with this subgroup usually progress to Secondary Progressive Multiple Sclerosis.

Secondary Progressive Multiple Sclerosis:

Like Primary Progressive, the symptoms of MS continually progress. In comparison to Relapse-Remitting MS, there is characteristically less inflammation and an increase in slow nerve damage in Secondary Progressive MS. Although the symptoms will begin to progress steadily, that does not necessarily mean that they will progress more quickly.

Progressive Relapsing Multiple Sclerosis:

This is the most rare form of MS, with only 5% of MS patients diagnosed as having Progressive Relapsing MS. For these patients, relapses occur periodically; however, symptoms continue and progress between relapses. Due to the progressive onset of Progressive-Relapsing MS, it may be initially diagnosed as Primary-Progressive; however, after a relapse occurs doctors often recognize and change their diagnosis to Progressive-Relapsing MS.

What causes relapses in MS? Well unfortunately, research hasn’t found the exact physiological triggers. However, stress, infections, post-pregnancy, and vaccinations have all been associated with relapses.

Sources:

Types of MS and MS Treatment Options. (n.d.) Multilpe Sclerosis: Better Questions Lead to Better Answers. Retrieved November 25, 2013 from http://www.multiplesclerosis.com/us/treatment.php

Exercising for 150 minutes each week may be the best treatment for Alzheimer's!!!

This article was recently published in Journal of Alzheimer’s disease. I thought it was interesting because it was done with people who have Alzheimer’s disease and not animals. This study also correlates with one of the papers we just looked at about how exercise can help neuroinflammation in mice carrying NSE/htau23.

Alzheimer’s disease is a neurodegenerative disease, which is caused by inflammation in the brain. Aging mostly causes this disease but stress has its major effects as well. This disease causes dementia and as it progresses it worsens over time. One of the reasons that are known to be one of the causes of this disease is the Tau protein abnormality. This abnormality causes dysfunction in the microtubules of neurons that starts malfunction in between neurons. This causes an immune reaction that increase inflammation in the brain and leads to worsening of the problem in time.

A study was recently done on a group of participants with early Alzheimer’s disease to see the effects of exercise on the progression of the disease. This study was done on two groups of people; 17 of which were diagnosed with Alzheimer’s disease and 18 people as control who were similar in age, gender, education, genetic risk and had similar medication use. The participants went through a moderate intensity exercise on a treadmill for 12 weeks. Then they were tested for a memory test and a list-learning task.

After the tests were done the patients had improved in fitness levels by 10% and had much improvement with the memory and list learning tests. They had improved brain activity in areas of their brains, which were used to diagnose them with Alzheimer’s disease.

I believe that exercise is one of the best remedies for most diseases. Instead of taking medications with many known and unknown side effects, one could exercise to prevent different illnesses. If 150 minutes (2 hours and 30 minutes) a WEEK can help an Alzheimer’s patient improve then it will help in many preventative ways!

The link:

http://www.medicalnewstoday.com/articles/264201.php

Whiteman, Honor. "Powerful effect of exercise' against Alzheimer." Exercising for 150 minutes each week may be the best treatment for Alzheimer's. (Aug, 2013): n. page. Web. 25 Nov. 2013. <http://www.medicalnewstoday.com/articles/264201.php>.

HSV-1 and -2, the culprit behind ß-Amyloid plaques in Alzheimer's Disease?!

Researchers at the University of Manchester's Faculty of Life Sciences have investigated the effect that the common Herpes Simplex Virus has on the brain. Their research has found that over 90% of the viral DNA manifests within ß-amyloid proteins and instigates the growth of the ß-amyloid sheaths in the brain's of patients with Alzeheimer's Disease. HSV-1 and -2 are neurotropic and neuroinvasive viruses, meaning that they are able to remain in the body by becoming dormant in the cell bodies of neurons, hiding from the immune system. According to the researchers, during the dormant stage of the HSV infection, the viruses cause enough damage to disintegrate the neuronal cells. Upon disintegration, they release amyloid, which further develop into sheaths when even more neuronal cells are destroyed. The team hypothesizes that antiviral drugs aimed to inhibit the effects of the virus could also inhibit the plaque formations caused by this virus.


Here is the link to the article:
http://www.sciencedaily.com/releases/2008/12/081207134109.htm

1.) University of Manchester. "Cold Sore Virus Linked To Alzheimer's Disease: New Treatment, Or Even Vaccine Possible." ScienceDaily, 7 Dec. 2008. Web. 22 Nov. 2013.

Compound found in marijuana may be a treatment for Alzheimer's disease

This article was published yesterday and talks about a very recent study that was done to see why anti-inflammatory drugs, like ibuprofen, essentially kill the 'buzz' from marijuana and suppress marijuana's negative effects on cognition. The point being that this may lead to new treatments for patients with Alzheimer's disease and other neurodegenerative diseases.

Marijuana has been shown to decrease inflammation in the brain, a big role in many neurodegenerative diseases. However, marijuana also can create a 'high' and long-term cognitive and memory effects that are probably not desired by patients with already deteriorating neurons. So, scientists are thinking that isolating the active compound from marijuana (THC) and supplementing it with an anti-inflammatory drug will stop the patient from getting the unwanted side effects!

They performed multiple experiment on AD mice to show that a combination of THC and COX inhibitors (anti-inflammatory) resulted in a decrease in beta-amyloid plaques and no lethargy that is usually seen with 'stoned' mice. Since this was only given over a couple of days though, I wonder how long-term chronic use of the combinations of drugs would affect cognition and memory.

I thought this article was really interesting (even if it is a lay article) so I recommend checking it out, even if you don't want to comment on it!!! The article also has the link to the research paper.

Here is the article:
http://www.latimes.com/science/sciencenow/la-sci-marijuana-ibuprofen-alzheimers-buzzkill-20131121,0,7844486.story#axzz2lPckqpnH

Niemann-Pick Type C

Last week, I had been thinking about how our next topic was neurodegenerative diseases. I was getting ready to read my Lay article and happened to be reading the Wall Street Journal at work before starting.  On the front page of the newspaper on Friday was an article that caught my eye. It was an article about children with Niemann-Pick disease Type C. It was funny to me that this article was in the newspaper this week so I thought I would make a blog post about it!

Niemann-Pick type C is an inherited neurodegenerative disorder of intracellular cholesterol and glycolipid trafficking defects. There are two genes that have been linked to the disease, NPC1 and NPC2.

The article is about a family who has twins with the disease. It explains how the twin girls became sick and had enlarged spleens which was diagnosed as mononucleosis at first. When the mono was gone and their spleens were still abnormal, doctors suspected a lysosomal storage disease marked by a failure of the cells to process and recycle waste. This disease gradually inhibits mobility, speech, and the ability to swallow. The rest of the article talks about the family and their journey in working with scientists to find a cure. There is a robot in one of the doctors labs that works around the clock to test new drugs on various diseases. It is really interesting!

Here is a link to the article online: http://projects.wsj.com/trials/#chapter=1

Marcus, Amy D. "Trials: Saving Kids, Changing Science." Wall Street Journal 15 Nov. 2013: A1+. Print.

Parkinson's Disease

This week, my Lay article was about how allergies may be linked to Parkinson's Disease (PD). I thought it would be a good idea to research PD a little more in depth. I found this really informational website about PD It has an overview of the disease and goes on to explain how it is diagnosed, the symptoms, treatment, and many other topics discussing how to live with it.

In the U.S. alone, there are over 50,000 new cases of PD diagnosed each year, over a million people who are already living with the disease, and six million worldwide. The CDC has rated complications from PD to be the 14th leading cause of death. PD is a neurodegenerative disorder of the brain. It is a slowly progressing disease and individuals PD can live with it for twenty years or more after diagnosis. The disease itself is not fatal, but there is no cure. Dopamine is a chemical that helps maintain smooth, coordinated muscle movements in humans. In PD, the neurons in the brain that produce dopamine in the substantial nigra become damaged and cannot produce enough dopamine. To diagnose PD, doctors look for four main symptoms: shaking, slowed movement, stiffness, and trouble with balance. There is no cure for PD, but there is therapy to treat the symptoms and ways to learn to live with the disease.

These were the main points that I found interesting from the website. Here is the link to the website for further learning!

www.Parkinson.org

"Parkinson's Disease Overview." National Parkinson Foundation. N.p., n.d. Web. 21 Nov. 2013.

Coffee, Caffeine, and Alzheimer's Disease?

     In class on Monday, we discussed that excitatory neurons have protective measures against an inflammation response. This is why many people suggest that older people continue to “use their brains” to keep new and old synapses firing. This also made me wonder what other ‘protective mechanisms’ are out there to slow down the progression of Alzheimer’s disease.

     Interestingly enough, I found this article about a connection between caffeine, coffee, and Alzheimer’s disease that was published in the Journal of Alzheimer’s Disease in June 2011. From previous studies that have found that daily coffee/caffeine intake during mid-life can decrease the risk of Alzheimer’s disease, researchers at the University of South Florida wanted to determine what exactly the coffee and caffeine were doing to the brain.  They already had found that the caffeine can cause a decrease in beta-amyloid production in the brain, but since other caffeinated drinks and decaffeinated coffee did not show decreased production of the protein, they were more interested in other ingredients in the coffee that could have an effect.

In their new study, they found that caffeinated coffee (and not other caffeinated drinks and de-caffeinated coffee) boosted blood levels of a growth factor called GCSF, granulocyte colony stimulating factor. This factor is important for recruiting bone marrow stem cells to move to the brain to remove the beta-amyloid proteins and increases new neuronal connections. Consequently, researchers believe that GCSF is associated with improved memory function and protecting against AD.

What was really interesting to me is that in order to get this beneficial protective effect, a person needs to consume 4 to 5 cups of coffee a day. Considering that the average person only drinks 1.5 to 2 cups a day, 4 to 5 cups seems a little excessive.

What do you all think? Is this a good avenue to pursue on preventing Alzheimer's disease? Coffee does have a lot of antioxidants that help reduce inflammation so could this maybe play a role in lowering the risk of AD as well?

Here is the article:

University of South Florida (USF Health). "Mystery ingredient in coffee boots protection against Alzheimer's disease, study finds." ScienceDaily. 28 Jun. 2011.

 

    

Gene Therapy for rheumatoid arthritis

When searching for what types of treatments are available for patients with rheumatoid arthritis, I came across an article about gene therapy. In regards to the article that I discussed last class, anti-IL-1 a/B and anti-TNF-a drugs are known to ameliorate the inflammatory process of RA. However one of the drawbacks of taking those medications is that individuals need to take them continuously. So since there are always advancements in technology, it would only make sense to gene therapy could be a potential treatment, right?  

Well according to the authors of this article, they felt that this approach would provide a more lasting effect in patients with RA via transplantation of genetically modified cells directly into the joint that is inflamed. It is reported that there have already been studies involving injections of IL-1Ra (an IL-1 inhibitor) into rabbits, mice, and rats showing that there is decreased toxicity, which lead to a phase I clinical trial where cells transfected with IL-Ra retrovirus were administered. These cells were rheumatoid arthritis synovial fibroblasts (RASF), which are cells that playing in a role in the initiation and perpetuation of the disease. It is proposed that once these cells are administered to the affected site, there would be a long-term safety outcome as the transfected cells would proliferate and inhibit inflammation.

But the ultimate question is, is this safe? The authors state that there are some pros and cons to this approach. In the phase 1 clinical trial, they state that the transduced cells were found only in the surface of the synovium (soft tissue around the joint capsule and joint cavity) in the metacarpal phalangeal joints of patients one week after administration of the cells. This is ideal because you would not want cells transducing their effects elsewhere in the body, which is obviously undesirable. Also in the study, there was a 5-year waiting period before reporting results of the study, which is important to help assess the efficacy of treatment long term. However, it was found in a patient receiving a high dosage of the cells led to migration of these cells in and adjacent control joint rather than localization to the affected, targeted area.

Overall, gene therapy appears to somewhat promising in treating those with rheumatoid arthritis due to emergence of studies such as transgene expression in those with the disease. Being that this article was published in 2005, it makes me wonder what other types of advancements have been done in the last 8 years and if gene therapy has been effective in treating humans with RA. Is it possible to have multiple joints treated at the same time? However, I feel in the end getting such treatments would be quite costly so only a certain demographic of people would be able to afford it.

Mountz, JD , J. Chen, and H-C Hsu. "Rheumatoid Arthritis: Safe and Sound." Gene Therapy 12 (2005): 1542-1543. Print.

What do people know about osteoarthritis?

As we all have discussed in class, osteoarthritis (OA) is the most common form of arthritis marked by the deterioration of the protective cartilage between joints, which leads to bones rubbing against each other resulting in swelling, pain, and decreased range of motion at the joint. Since it is one of the most common forms of arthritis affecting millions worldwide, I found one particular article quite interesting. The main focus of the article was to evaluate the level of knowledge that patient’s with OA knew about the condition.

Nonetheless, the study was conducted into 3 phases. The first phase was used to develop the questionnaire by having one-on-one interviews between 12 consecutive patients (both male and female) diagnosed with symptomatic OA of any joint at a rheumatology outpatient clinic to determine what questions would be suitable for the questionnaire. With this information, a 16 multiple choice question test was formed and examined by a team of health professionals, in which questions were divided under disease process, drug therapies (common meds and side effects), rest and exercise methods, and joint protection and additional therapies. Then phase 2 was a pilot study that was then conducted in a rheumatology outpatient department with 30 consecutive both male and female patients from 5 clinics to assess readability and reproducibility. A final second copy of the test was reproduced to give to 83 patients in phase 3, which consisted of 22 males and 61 females. Patients were scored on each sub-group individually and in total of their knowledge in the questionnaire.

As a result, in the questions regarding the disease process, a vast majority understood the disease knew main symptoms of the disease and diagnosis, but I thought it was interesting that 20% of patients (17 of them) thought that OA was a condition caused by cold, damp weather.  In the other groups of questions listed I also thought it was interesting that there were about a quarter of patients that chose the “I don’t know option”, which is a bit concerning considering the fact that those categories involve questions regarding therapies and treatment of OA. I would think that individuals with the disease would at least know some information to an extent to alleviate the pain and other symptoms that they would be experiencing with OA. Overall, the authors felt that indeed patients require more information and this is publicly available in an assortment of handbooks. They suggest other techniques such as providing drug information leaflets or educational sessions to address the information.

Hill, J., and H. Bird. "Patient knowledge and misconceptions of osteoarthritis assessed by a validated self-completed knowledge questionnaire (PKQ-OA)."Rheumatology 46 (2006): 796-800. Print.