Monday, September 22, 2008
Is Parkinson's Disease Inherited?
Is Parkinson's Disease Inherited? That was the question I asked back in 1993 to one of my neurobiology professors, a Parkinson's expert and researcher. On that day he told me definitively, "No." Even back then, 15 years ago, I suspected he was wrong. I really thought that there was probably some sort of genetic connection that was not understood at all.
Today scientists believe that there is a genetic connection, in fact, they have identified several mutations that can give rise to Parkinson's Disease. That being said, scientists estimate that less than 25% of all PD cases are genetically linked and they also believe that not all those with the gene mutations develop PD.
The information about familial (genetic) Parkinson's is actually quite extensive now. (Isn't it amazing what we have learned in 15 years?) Now scientists have numerous genetic suspects. Here is a summary of some of the most prevalent.
1. LRRK2 (leucine-rich repeat kinase)- This gene is a dominant gene, meaning that a person only needs one copy of this gene in order for it to be expressed in an individual. Scientists have identified at least 20 mutations in families that exhibit late onset PD. This genetic "flaw" is the most common form of Parkinson's as far as scientists know at this time. This is the genetic mutation that Sergey Brin identified in his gene make up.
2. GIGYF2- Mutations on this gene are known to cause a single amino acid substitution in the protein this gene encodes for. What does this mean? Essentially one link in the chain of a protein is swapped out for a different kind of link which then leads to the protein being formed incorrectly. The interesting aspect of this genetic mutation is that it is also assoicated wiht Insulin production. Scientists aren't sure, but they think there might be a connection between PD and Insulin and thereby possibly diabetes. There are now ongoing studies to try to piece together how these diseases are inter-related, if at all.
3. A study of a handful of French families with Parkinson's uncovered that duplications in the gene that creates the alpha-synuclein protein may cause PD. It is known that alpha-synuclein protein is a major component of Lewy Bodies, an abnormal "clump" of proteins that form inside nerve cells. The French study showed that a duplication of this gene caused PD similar to other types of PD, but that a triplication of the same gene caused a devastating form of PD with an average onset of 34 and a rapid decline into dementia. I know from reading other articles in the past that there is a big push to look into whether or not limiting or removing "extra" alpha-synuclein could slow the progression of PD.
4. LI66P mutation- This particular mutation is linked to an early onset form of familial PD. It is thought that this mutation disrupts DJ-1 protein folding. By disrupting folding of a protein this mutation would essentially render the DJ-1 protein useless and upset the functions that it performs in the body. LI66P is recessive so someone would have to receive the same gene mutation from both parents in order to have its affects exhibit.
There are several other genetic mutations that are linked to PD, but I think 4 is enough for any one blog posting. Just because someone has one of these mutations does not appear to be enough to develop Parkinson's Disease. It is thought that the genetic mutations, at least for the most part, make someone more susceptible, but that some sort of environmental trigger needs to occur as well for a person to develop the disease. The exact mechanisms are not known.
So I now have a question- if PD ran in your family would you want to know if you had any of these genetic factors if there was nothing to do to prevent the disease? PD does run in my family, my Mom, my Grandpa, but as of now I have no desire to have any genetic tests done. That may change in the future especially if preventative methods are developed. Only time will tell.
Friday, September 19, 2008
Have You 'Googled' Parkinson's Disease Recently
If you 'Google' Parkinson's Disease today the item in the 4th position is about Google Co-Founder, Sergey Brin. This fact may not be news to most people in the Parkinson's Community as Mr. Brin is all over the PD news today. Unfortunately his mother and her aunt have PD. I saw an article earlier this week about his family, his mother's PD and the fact that the Brin family has endowed a professorship at the University of Maryland. It caught my eye since a co-founder of Google being interested in curing Parkinson's can only help my cause. However, this act of advocacy, kindness, charity, or whatever appropriate word we use, is not the reason for all the hubbub surrounding Mr. Brin and Parkinson's. The reason for the NUMEROUS news stories is that Mr. Brin started his own blog and his post from yesterday is about Parkinson's Disease and his family.
In his blog posting he reveals that through the genetic testing of his wife's company, 23andMe, he discovered that he has a genetic mutation which raises his risk for developing Parkinson's. The LRRK2 gene with the known mutation, G2019S, is a marker for the disease although not everyone with this mutation will develop PD. His mother also has this genetic mutation. It is thought that familial PD is relative rare, but there are definitely instances of several family members across generations developing Parkinson's.
I was very interested in all the news surrounding Brin's PD disclosure. First, Parkinson's "runs in my family" so obviously I have an interest in a possible genetic pre-disposition. I would love for science to be able to tell how much of this disease is genetic and how much is environmental or other factors. No one knows this information yet and the thoughts around this subject vary greatly among experts. (I have read anything I can find on this subject and the experts definitely do not agree.)
Second, I am fascinated that the blog entry is what "made the news". I only came across one article earlier this week about the Brin family endowing the professorship yet the blog entry is all over the web already. (I guess I am adding to that.)
I applaud Sergey Brin for allowing for his personal family matters to become somewhat public. I have no doubts it is not easy for someone in the public eye to share personal information so publicly. I also applaud his entire family for taking steps to find a cure and give back to the world at large. I hope that his tie to Parkinson's will help get us closer to a cure.
To read Sergey Brin's blog click on this link.
http://too.blogspot.com
In his blog posting he reveals that through the genetic testing of his wife's company, 23andMe, he discovered that he has a genetic mutation which raises his risk for developing Parkinson's. The LRRK2 gene with the known mutation, G2019S, is a marker for the disease although not everyone with this mutation will develop PD. His mother also has this genetic mutation. It is thought that familial PD is relative rare, but there are definitely instances of several family members across generations developing Parkinson's.
I was very interested in all the news surrounding Brin's PD disclosure. First, Parkinson's "runs in my family" so obviously I have an interest in a possible genetic pre-disposition. I would love for science to be able to tell how much of this disease is genetic and how much is environmental or other factors. No one knows this information yet and the thoughts around this subject vary greatly among experts. (I have read anything I can find on this subject and the experts definitely do not agree.)
Second, I am fascinated that the blog entry is what "made the news". I only came across one article earlier this week about the Brin family endowing the professorship yet the blog entry is all over the web already. (I guess I am adding to that.)
I applaud Sergey Brin for allowing for his personal family matters to become somewhat public. I have no doubts it is not easy for someone in the public eye to share personal information so publicly. I also applaud his entire family for taking steps to find a cure and give back to the world at large. I hope that his tie to Parkinson's will help get us closer to a cure.
To read Sergey Brin's blog click on this link.
http://too.blogspot.com
Wednesday, September 17, 2008
Parkinson's Disease Edaravone Study
An article published in the journal BMC Neuroscience in the August 2008 edition caught my eye this week. The article was about a compound called edaravone (chemical name- 3-methyl-1-phenyl-2-pyrazolin-5-one) that is used in ischemic stroke patients to protect neurons in the brain. Scientists think that edaravone may be neuroprotective because it will scavenge free radicals in the brain. The researchers in this study thought that this neuroprotective behavior might help in Parkinson’s Disease.
So what’s a free radical exactly? (No, it’s not a political extremist running amok in society as my husband likes to say every time I say something about free radicals and PD.) Free radicals are molecules that have an “extra” electron that is not paired with another electron. This “extra” electron does not like being unpaired so it looks for other molecules that it can “take” electrons from. When a free radical “takes” these electrons it can cause a host of issues for the “donor” molecule including cell death. Obviously the more free radicals that exist in someone’s brain the more cells that can be adversely affected. Edaravone is thought to essentially “eat up” these free radicals by binding with the “extra” electrons itself.
Now on to the actual study and how edaravone may help Parkinson’s Disease.
The study was conducted in two phases. First a known dopamine neuron toxin called 6-OHDA (6-hydroxydopamine) was applied to cells in-vitro (outside of a living organism) and then either edaravone or regular old saline was applied to the cells and the number and/or concentration of dopamine neurons was measured to see which group contained more dopamine cells. Second, an animal model of PD was used. In the second phase 6-OHDA was injected into several rats’ brains and then either edaravone or saline was administered intravenously at one of two different time periods. The first group received either edaravone or saline 30 minutes after the 6-OHDA injection and the second was administered edaravone or saline 24 hours after the initial 6-OHDA injection. The study was looking at two things: 1) Did the edaravone rats maintain more dopamine neurons than the saline rats and 2) Did those who received the edaravone at 30 minutes maintain more dopamine than those who received it at 24 hours.
The results of the study bode well for edaravone helping to protect dopamine neurons. First, the in-vitro part of the study showed a statistically significant increase in the number of surviving dopamine neurons in the edaravone infused cells over the saline infused controls. Second, the rats that received edaravone at either 30 minutes or 24 hours both had statistically significant higher amounts of dopamine cells when measured against those rats that only received saline. Also, those rats that received the edaravone at 30 minutes had statistically significant more dopamine neurons than those that received the same dosage at 24 hours.
The study’s authors concluded that edaravone did three things that might protect cells. First, it decreased oxidative stress by scavenging those nasty free radicals. Second, it decreased apoptosis (essentially cell suicide) and lastly it decreased inflammation in the brain.
So what implications does this have for Parkinson’s Disease? At this moment, not a lot, but possibly over a few years this compound could be used to help delay onset or help slow progression by “eating up” free radicals. Edaravone might also be helpful by increasing the survival of transplanted stem cells by decreasing apoptosis (cell suicide) and it might help decrease the inflammatory reaction due to surgery in the brain. All of these avenues offer hope for potential drugs or PD treatments that could help millions of Parkinson’s patients in the future. I will be watching for updates on edaravone and any applications it may have to Parkinson’s Disease.
As always here is a link to the study. A link to the full article is at the end of this abstract.
Edaravone Study
So what’s a free radical exactly? (No, it’s not a political extremist running amok in society as my husband likes to say every time I say something about free radicals and PD.) Free radicals are molecules that have an “extra” electron that is not paired with another electron. This “extra” electron does not like being unpaired so it looks for other molecules that it can “take” electrons from. When a free radical “takes” these electrons it can cause a host of issues for the “donor” molecule including cell death. Obviously the more free radicals that exist in someone’s brain the more cells that can be adversely affected. Edaravone is thought to essentially “eat up” these free radicals by binding with the “extra” electrons itself.
Now on to the actual study and how edaravone may help Parkinson’s Disease.
The study was conducted in two phases. First a known dopamine neuron toxin called 6-OHDA (6-hydroxydopamine) was applied to cells in-vitro (outside of a living organism) and then either edaravone or regular old saline was applied to the cells and the number and/or concentration of dopamine neurons was measured to see which group contained more dopamine cells. Second, an animal model of PD was used. In the second phase 6-OHDA was injected into several rats’ brains and then either edaravone or saline was administered intravenously at one of two different time periods. The first group received either edaravone or saline 30 minutes after the 6-OHDA injection and the second was administered edaravone or saline 24 hours after the initial 6-OHDA injection. The study was looking at two things: 1) Did the edaravone rats maintain more dopamine neurons than the saline rats and 2) Did those who received the edaravone at 30 minutes maintain more dopamine than those who received it at 24 hours.
The results of the study bode well for edaravone helping to protect dopamine neurons. First, the in-vitro part of the study showed a statistically significant increase in the number of surviving dopamine neurons in the edaravone infused cells over the saline infused controls. Second, the rats that received edaravone at either 30 minutes or 24 hours both had statistically significant higher amounts of dopamine cells when measured against those rats that only received saline. Also, those rats that received the edaravone at 30 minutes had statistically significant more dopamine neurons than those that received the same dosage at 24 hours.
The study’s authors concluded that edaravone did three things that might protect cells. First, it decreased oxidative stress by scavenging those nasty free radicals. Second, it decreased apoptosis (essentially cell suicide) and lastly it decreased inflammation in the brain.
So what implications does this have for Parkinson’s Disease? At this moment, not a lot, but possibly over a few years this compound could be used to help delay onset or help slow progression by “eating up” free radicals. Edaravone might also be helpful by increasing the survival of transplanted stem cells by decreasing apoptosis (cell suicide) and it might help decrease the inflammatory reaction due to surgery in the brain. All of these avenues offer hope for potential drugs or PD treatments that could help millions of Parkinson’s patients in the future. I will be watching for updates on edaravone and any applications it may have to Parkinson’s Disease.
As always here is a link to the study. A link to the full article is at the end of this abstract.
Edaravone Study
Monday, September 15, 2008
Stem Cells and Parkinson's Disease
Stem cells have long been in the news as a potential therapy or possible cure for Parkinson's Disease. So what exactly are stem cells? First you should know that there are several different types of stem cells. The two types that are mentioned most often are embryonic stem cells and adult stem cells. There are other types, but let's stick to these two.
A stem cell is a cell that has three basic properties:
1. It can "renew" or regenerate itself for a much longer period of time than regular cells in the body,
2. It is unspecialized- meaning that it has not "chosen" a specific tissue type, i.e.- heart muscle, brain tissue, liver cell,
3. It has the ability to specialize- meaning it can become a specific type of tissue and take on that tissue's role in the body.
An embryonic stem cell is an undifferentiated (unspecified) cell from a 5-day old pre-implementation embryo.
An adult stem cell (aka somatic cell) is also an undifferentiated cell but these cells come from many types of tissue, bone marrow, brain tissue, etc. There is no embryo involved in these types of cells.
So what's all the debate about? Well, during the extraction of embryonic stem cells the embryo itself is generally destroyed. This risk raises the ehtical/moral questions about whether or not the procedure is destroying life or advancing science. Adult stem cells can also be used for research and possibly therapies, but it is not well known if adult stem cells can differentiate into all the cell types in the body. Embryonic stem cells are more versatile in that they can become most, if not all, types of cells in the body. However, adult stem cells are not rejected after implantation as they are from the patient's body already.
Until recently it seemed like both embryonic and adult stem cells both had advantages and that the moral and political debate would continue for years. Then something amazing happened back in November 2007, two scientists working separately were able to turn ordinary human skin cells into what could effectively be considered embryonic stem cells. The scientists took regular human skin cells and with the help of some genetically engineered viruses were able to transform the skin cells into embryo-like stem cells. Their method used four genes in a proper sequence to make the skin cells almost indistinguishable from embryonic stem cells.
This new finding breaks open the entire stem cell research world. Now there is a way to take regular cells, without hurting anyone or anything, and turn it into essentially embryonic stem cells. With any luck this method will allow for vastly increased ways to study embryonic stem cell, develop new therapies using them and also increase federal funding for these lines of research.
I will of course be watching for further developments in this research as it holds out hope for a cure or at least better therapies for Parkinson's Disease. When I find further research in this area believe me that it will be posted.
A stem cell is a cell that has three basic properties:
1. It can "renew" or regenerate itself for a much longer period of time than regular cells in the body,
2. It is unspecialized- meaning that it has not "chosen" a specific tissue type, i.e.- heart muscle, brain tissue, liver cell,
3. It has the ability to specialize- meaning it can become a specific type of tissue and take on that tissue's role in the body.
An embryonic stem cell is an undifferentiated (unspecified) cell from a 5-day old pre-implementation embryo.
An adult stem cell (aka somatic cell) is also an undifferentiated cell but these cells come from many types of tissue, bone marrow, brain tissue, etc. There is no embryo involved in these types of cells.
So what's all the debate about? Well, during the extraction of embryonic stem cells the embryo itself is generally destroyed. This risk raises the ehtical/moral questions about whether or not the procedure is destroying life or advancing science. Adult stem cells can also be used for research and possibly therapies, but it is not well known if adult stem cells can differentiate into all the cell types in the body. Embryonic stem cells are more versatile in that they can become most, if not all, types of cells in the body. However, adult stem cells are not rejected after implantation as they are from the patient's body already.
Until recently it seemed like both embryonic and adult stem cells both had advantages and that the moral and political debate would continue for years. Then something amazing happened back in November 2007, two scientists working separately were able to turn ordinary human skin cells into what could effectively be considered embryonic stem cells. The scientists took regular human skin cells and with the help of some genetically engineered viruses were able to transform the skin cells into embryo-like stem cells. Their method used four genes in a proper sequence to make the skin cells almost indistinguishable from embryonic stem cells.
This new finding breaks open the entire stem cell research world. Now there is a way to take regular cells, without hurting anyone or anything, and turn it into essentially embryonic stem cells. With any luck this method will allow for vastly increased ways to study embryonic stem cell, develop new therapies using them and also increase federal funding for these lines of research.
I will of course be watching for further developments in this research as it holds out hope for a cure or at least better therapies for Parkinson's Disease. When I find further research in this area believe me that it will be posted.
Friday, September 12, 2008
Parkinson's Disease Caregivers
Today I am going to write about caregivers of people with Parkinson's. As usual when I decided this was the topic I wanted to write about I did some research on the Internet to see what sites and information already exists in the ethernet. To my surprise there was remarkably little information and only a couple of sites that seemed to focus on the caregiver at all. Now, I think that is something that I will have to work to change in the future. Obviously I will not change that in one blog posting so I will not try.
The one site I came across that seemed to have a lot of information and a good forum for caregivers and/or patients to share information is:
www.myparkinsons.org
This site has some useful information for caregivers, links to MANY other parkinson's sites, but what seemed the most useful in my mind was the forum. There were numerous postings and it definitely appears that the site has a true community that will try to answer questions that you have.
I personally think that caring for someone who has PD must be very difficult, especially as the patient's health begins to decline. My Mom has PD and my Dad is the primary caregiver so I do not know exactly how tough it is, but I am sure it is not easy.
In general the caregiver information out there all seems to say the same thing: get informed, stay informed, and make sure to take some time for yourself as well. I think that is all good advice.
To all the caregivers I wish you luck and salute you for your fight against Parkinson's Disease in whatever way you do it.
The one site I came across that seemed to have a lot of information and a good forum for caregivers and/or patients to share information is:
www.myparkinsons.org
This site has some useful information for caregivers, links to MANY other parkinson's sites, but what seemed the most useful in my mind was the forum. There were numerous postings and it definitely appears that the site has a true community that will try to answer questions that you have.
I personally think that caring for someone who has PD must be very difficult, especially as the patient's health begins to decline. My Mom has PD and my Dad is the primary caregiver so I do not know exactly how tough it is, but I am sure it is not easy.
In general the caregiver information out there all seems to say the same thing: get informed, stay informed, and make sure to take some time for yourself as well. I think that is all good advice.
To all the caregivers I wish you luck and salute you for your fight against Parkinson's Disease in whatever way you do it.
Wednesday, September 10, 2008
Parkinson’s Disease and Sonic Hedgehog
You read the title of this post correctly! Now you’re asking what the heck do Parkinson’s Disease and Sonic the Hodgehog have in common? Well, the disease and the video game have nothing in common, but a brain protein named after the video game is being linked to the disease. That’s right there is a protein in your brain named Sonic Hedgehog (shh) that is implicated in Parkinson’s Disease. I thought I was reading something wrong when I first read an article about Sonic Hedgehog, but I was not wrong and this was no joke.
There are a group of brain proteins called hedgehogs of which Sonic Hedgehog is one. The role of shh is seen during embryogenesis (embryo growth) and spurs development of dopaminergic neurons in the basal ganglia section of the brain which is affected in PD. The protein is now known to exist in the adult brain too.
The name alone inspired me to learn more about this protein so I began searching the Internet for different articles about this uniquely named molecule. What I found was an entire body of knowledge and study about this “hedgehog” protein. It turns out that there are three separate avenues of study of shh in Parkinson’s.
First, researchers are looking at whether this protein could cause adult stem cells in the brain to differentiate into (become) dopamine producing neurons. Obviously being able to grow more dopaminergic neurons in the affected areas in patients with PD would help tremendously. Researchers are still working on this avenue of study in animals. Time will tell if this has efficacy in humans.
The second avenue of research explores applying shh directly into the basal ganglia. It appears that shh can work as an actual neurotransmitter in the brain and when applied to the basal ganglia in animal studies the amount of electrical activity in the subthalamic nucleus decreased. Since the subthalamic nucleus is hyperactive in PD, a compound that decreases this activity would be a possible treatment. Again, this line of research is being pursued, but human results are not known at this time.
Lastly, several researchers explored the neuroprotective properties of Sonic Hedgehog and also another protein, Gli-1. They delivered both of these compounds to the brain via a genetically engineered virus. What they found was that both of these proteins appear to protect neurons and prevent neuronal loss as compared to other controls. Sonic saves the day!
I started reading about Sonic Hedgehog because I found the name amusing and thought it was great that neuroscientists have a wonderful sense of humor. What I found was 3 different paths of research about this one compound. I am still amazed that researchers can take one particular protein and then can find 3 completely different potential ways that this protein can help in a disease like Parkinson’s. None of these avenues have led to clinical applications yet, but that does not mean that one or all won’t in the future.
There are a group of brain proteins called hedgehogs of which Sonic Hedgehog is one. The role of shh is seen during embryogenesis (embryo growth) and spurs development of dopaminergic neurons in the basal ganglia section of the brain which is affected in PD. The protein is now known to exist in the adult brain too.
The name alone inspired me to learn more about this protein so I began searching the Internet for different articles about this uniquely named molecule. What I found was an entire body of knowledge and study about this “hedgehog” protein. It turns out that there are three separate avenues of study of shh in Parkinson’s.
First, researchers are looking at whether this protein could cause adult stem cells in the brain to differentiate into (become) dopamine producing neurons. Obviously being able to grow more dopaminergic neurons in the affected areas in patients with PD would help tremendously. Researchers are still working on this avenue of study in animals. Time will tell if this has efficacy in humans.
The second avenue of research explores applying shh directly into the basal ganglia. It appears that shh can work as an actual neurotransmitter in the brain and when applied to the basal ganglia in animal studies the amount of electrical activity in the subthalamic nucleus decreased. Since the subthalamic nucleus is hyperactive in PD, a compound that decreases this activity would be a possible treatment. Again, this line of research is being pursued, but human results are not known at this time.
Lastly, several researchers explored the neuroprotective properties of Sonic Hedgehog and also another protein, Gli-1. They delivered both of these compounds to the brain via a genetically engineered virus. What they found was that both of these proteins appear to protect neurons and prevent neuronal loss as compared to other controls. Sonic saves the day!
I started reading about Sonic Hedgehog because I found the name amusing and thought it was great that neuroscientists have a wonderful sense of humor. What I found was 3 different paths of research about this one compound. I am still amazed that researchers can take one particular protein and then can find 3 completely different potential ways that this protein can help in a disease like Parkinson’s. None of these avenues have led to clinical applications yet, but that does not mean that one or all won’t in the future.
Tuesday, September 9, 2008
Pain and Parkinson's Disease
A new research study conducted in Italy is making the news today. The study looked at the incidence of pain reported by Parkinson’s patients versus a normal control group. I found this study interesting because it shows that researchers are recognizing that there are symptoms besides motor symptoms that may lead to quality of life issues or may help diagnose the disease easier. In my opinion this study is not a huge breakthrough in that it is not a bug leap closer to a cure, but all new knowledge does help move us collectively closer to the goal of a cure.
The researchers started the study with the hypothesis that pain is associated with Parkinson’s at clinical onset or at some point thereafter. The study divided pain into 2 categories: dystonic and non-dystonic pain. The first type, dystonic, is characterized as painful sensations, often described as cramping or arthritis and is caused by involuntary muscle contractions. Non-dystonic pain is essentially pain with the absence of dystonic pain. What the researchers found was that pain associated with dystonia was statistically higher in PD patients versus the control group. (69.9% vs 62.8%, p=0.04) The researchers also found that non-dystonic pain was not statistically higher for Parkinson’s patients, but the occurrence of non-dystonic pain was correlated to the onset of clinical Parkinson’s.
All of this information is overall interesting even if I don’t see a direct application to immediate better treatments or a cure. To me what this means is that doctors should pay attention to unexplained, dystonic pain and keep Parkinson’s as a possible diagnosis in the back of their minds. I have a feeling that many people with Young Onset Parkinson’s that present with pain as one of their main symptoms will have many tests to rule out a host of other possible causes before a PD diagnosis is made. I have no doubt that going through all the tests must be aggravating to say the least.
To read the abstract of this study from the Archives of Neurology click this link.
http://archneur.ama-assn.org/cgi/content/short/65/9/1191
The researchers started the study with the hypothesis that pain is associated with Parkinson’s at clinical onset or at some point thereafter. The study divided pain into 2 categories: dystonic and non-dystonic pain. The first type, dystonic, is characterized as painful sensations, often described as cramping or arthritis and is caused by involuntary muscle contractions. Non-dystonic pain is essentially pain with the absence of dystonic pain. What the researchers found was that pain associated with dystonia was statistically higher in PD patients versus the control group. (69.9% vs 62.8%, p=0.04) The researchers also found that non-dystonic pain was not statistically higher for Parkinson’s patients, but the occurrence of non-dystonic pain was correlated to the onset of clinical Parkinson’s.
All of this information is overall interesting even if I don’t see a direct application to immediate better treatments or a cure. To me what this means is that doctors should pay attention to unexplained, dystonic pain and keep Parkinson’s as a possible diagnosis in the back of their minds. I have a feeling that many people with Young Onset Parkinson’s that present with pain as one of their main symptoms will have many tests to rule out a host of other possible causes before a PD diagnosis is made. I have no doubt that going through all the tests must be aggravating to say the least.
To read the abstract of this study from the Archives of Neurology click this link.
http://archneur.ama-assn.org/cgi/content/short/65/9/1191
Monday, September 8, 2008
Depression in Parkinson's Disease
The link between Parkinson's Disease and depression has come to light more in the past 5 years or so. Researchers are finally beginning to notice that depression occurs in a large part of the PD population (estimates are 40-50%).
The exact reasons for why such a large portion of Parkinson's patients develop depression are not entirely known. It is thought that the biochemical alterations are a large culprit, but stess and psycho-social reasons probably play a role too. I am sure that people on hearing their diagnosis of PD are less than happy and may experience some level of depression for a while, but when does this depression cross the line from feeling down about a difficult disease into a clinical depression? Also, there is evidence that 12-37% of patients with depressive symptoms develop these symptoms prior to developing motor symptoms. Does this mean that the depression is mostly biochemical? I do not know.
How do you piece apart the chemical changes in a person's brain from the psycho-social or stress induced changes in someone's attitude or behavior? This is a question that I think will take years to answer, if it is able to be answered at all.
Since there is a large population of depression in PD you would think that treatments would be fairly well understood. That is not true at all and actually the opposite is closer to the truth. From the research I have read there are several anti-depressants that are possible for treatment, but none of them have significant research surrounding their use and efficacy in treating depression in Parkinson's. That being said, an anti-depressant may be the right choice for many patients. A motor disease specialist should be able to recommend some medications as possible treatments.
Besides anti-depressants a patient suffering from depression may want to consider other forms of treatments either jointly with anti-depressants or by themselves. Obviously qualified medical personnel should help the patient with any of these decisions. Some possibilities for treatments are: counseling, stress-management, relaxation techniques, coping strategies or support groups.
It is important to note that although Parkinson's is a difficult disease for all patients those with depression may suffer from a lower quality of life. It is important to work closely with the medical community to monitor the patient's mood and to help if warranted. Remember not all PD patients suffer from depression, but those that do may need help seeking treatment.
The exact reasons for why such a large portion of Parkinson's patients develop depression are not entirely known. It is thought that the biochemical alterations are a large culprit, but stess and psycho-social reasons probably play a role too. I am sure that people on hearing their diagnosis of PD are less than happy and may experience some level of depression for a while, but when does this depression cross the line from feeling down about a difficult disease into a clinical depression? Also, there is evidence that 12-37% of patients with depressive symptoms develop these symptoms prior to developing motor symptoms. Does this mean that the depression is mostly biochemical? I do not know.
How do you piece apart the chemical changes in a person's brain from the psycho-social or stress induced changes in someone's attitude or behavior? This is a question that I think will take years to answer, if it is able to be answered at all.
Since there is a large population of depression in PD you would think that treatments would be fairly well understood. That is not true at all and actually the opposite is closer to the truth. From the research I have read there are several anti-depressants that are possible for treatment, but none of them have significant research surrounding their use and efficacy in treating depression in Parkinson's. That being said, an anti-depressant may be the right choice for many patients. A motor disease specialist should be able to recommend some medications as possible treatments.
Besides anti-depressants a patient suffering from depression may want to consider other forms of treatments either jointly with anti-depressants or by themselves. Obviously qualified medical personnel should help the patient with any of these decisions. Some possibilities for treatments are: counseling, stress-management, relaxation techniques, coping strategies or support groups.
It is important to note that although Parkinson's is a difficult disease for all patients those with depression may suffer from a lower quality of life. It is important to work closely with the medical community to monitor the patient's mood and to help if warranted. Remember not all PD patients suffer from depression, but those that do may need help seeking treatment.
Friday, September 5, 2008
What Do You Want in a Post?
In thinking about my Parkinson's blog post for today I decided that I would love to know exactly what types of topics are of interest to readers so that I can blog about those topics more. So I have a favor to ask. Can you please let me know what topics interest you by leaving a comment on this blog post? If you'd rather email me instead please visit my Profile page and click on the email link.
Let me know if you are interested in postings about PD medications, fundraising or volunteer work, political advocacy, information about the mechanisms behind Parkinson's Disease or something else? I'd love to "hear" your thoughts.
I'm very interested in how to better provide valuable information for the Parkinson's community.
Have a great weekend!
Let me know if you are interested in postings about PD medications, fundraising or volunteer work, political advocacy, information about the mechanisms behind Parkinson's Disease or something else? I'd love to "hear" your thoughts.
I'm very interested in how to better provide valuable information for the Parkinson's community.
Have a great weekend!
Thursday, September 4, 2008
Protein Link Between Parkinson’s and Alzheimer’s
I think it is safe to say that everyone knows what Protein is at least in terms of food and nutrition, but not everyone might realize how much different protein molecules play vital roles in our bodies and in our brains.
First, exactly what is a protein at the molecular level? A fairly simple definition is that proteins are strings of amino acids that our bodies get from food and/or make themselves. These “strings” can then “fold” in several different ways and also interact with other proteins. A reasonable visual representation would be to think of them as a string of beads (amino acids) that is folded around itself and interwoven with other strings of beads. Obviously this is a fairly simplified example, but I think it gets the picture across.
Now, what does this have to do with Parkinson’s Disease or Alzheimer’s Disease? Well, proteins play many roles in our bodies, from forming muscles to helping neurons to communicate in our brains. In PD a particular protein, a-synuclein, is proposed to play a critical role in the formation of Lewy Bodies, a tell-tale sign of PD. Lewy Bodies are essentially the accumulation of a bunch of a-synuclein proteins and are known to cause disruption to neurons. In Alzheimer’s the Abeta amyloid protein is implicated in the formation of plaques which in turn cause the neurological difficulties experienced by Alzheimer’s patients. It is known clinically that a person who develops either PD or Alzheimer's is at a significantly higher risk to develop the other disease.
A new study conducted at the University of California at San Diego used super computers to help analyze how these two specific proteins interact and to explore why people with either Alzheimer’s or Parkinson’s disease have a higher risk for also developing the other neurological disorder. The researchers discovered that abnormal interactions between a-synuclein and Abeta amyloid can lead to the creation of “hybrid” complexes which result in a combination of Alzheimer’s and Parkinson’s. Using the computer models researchers were able to see the new hybrid protein form with a small hole called a “nanopore”. This hybrid disrupts neuronal activity.
The interesting part of this finding to me is that researchers have now shown at least one clear path of how Parkinson’s and Alzheimer’s are related in a molecular way. To me this finding clearly shows how solving the puzzle of one disease will have a dramatic impact on the other. If such a clear connection can be shown in these two diseases what other connections are there to other neurological disorders like ALS, MS, Huntington’s Disease, etc? How do we unlock the mystery of any of these diseases so that we can then solve all of the others? I am still convinced that curing or preventing one of these many diseases will be the key to curing them all.
As always here is the link to the study.
http://www.sciencedaily.com/releases/2008/09/080903204225.htm
First, exactly what is a protein at the molecular level? A fairly simple definition is that proteins are strings of amino acids that our bodies get from food and/or make themselves. These “strings” can then “fold” in several different ways and also interact with other proteins. A reasonable visual representation would be to think of them as a string of beads (amino acids) that is folded around itself and interwoven with other strings of beads. Obviously this is a fairly simplified example, but I think it gets the picture across.
Now, what does this have to do with Parkinson’s Disease or Alzheimer’s Disease? Well, proteins play many roles in our bodies, from forming muscles to helping neurons to communicate in our brains. In PD a particular protein, a-synuclein, is proposed to play a critical role in the formation of Lewy Bodies, a tell-tale sign of PD. Lewy Bodies are essentially the accumulation of a bunch of a-synuclein proteins and are known to cause disruption to neurons. In Alzheimer’s the Abeta amyloid protein is implicated in the formation of plaques which in turn cause the neurological difficulties experienced by Alzheimer’s patients. It is known clinically that a person who develops either PD or Alzheimer's is at a significantly higher risk to develop the other disease.
A new study conducted at the University of California at San Diego used super computers to help analyze how these two specific proteins interact and to explore why people with either Alzheimer’s or Parkinson’s disease have a higher risk for also developing the other neurological disorder. The researchers discovered that abnormal interactions between a-synuclein and Abeta amyloid can lead to the creation of “hybrid” complexes which result in a combination of Alzheimer’s and Parkinson’s. Using the computer models researchers were able to see the new hybrid protein form with a small hole called a “nanopore”. This hybrid disrupts neuronal activity.
The interesting part of this finding to me is that researchers have now shown at least one clear path of how Parkinson’s and Alzheimer’s are related in a molecular way. To me this finding clearly shows how solving the puzzle of one disease will have a dramatic impact on the other. If such a clear connection can be shown in these two diseases what other connections are there to other neurological disorders like ALS, MS, Huntington’s Disease, etc? How do we unlock the mystery of any of these diseases so that we can then solve all of the others? I am still convinced that curing or preventing one of these many diseases will be the key to curing them all.
As always here is the link to the study.
http://www.sciencedaily.com/releases/2008/09/080903204225.htm
Wednesday, September 3, 2008
New Finding with Deep Brain Stimilation
Could Deep Brain Stimulation(DBS) Stop the Progression of Parkinson's Disease???? Researchers at the University of Cincinnati and University Hospital are saying "Yes". A new study conducted by Caryl Sortwell, PhD and Michael Behbehani, PhD suggests that with a certain percentage of DBS patients that is the case. The study indicates that a protein in the brain called BDNF (brain-derived neurotrophic factor) is increased by the technique. This protein is known to be a tropic factor that provides "a nurturing, growth chemical" and it is thought that it may be responsible for the slow down in progression that some patients exist.
The study does note that not all patients seem to have the same results from DBS. Some patients have a marked decrease in symptoms and a slower progression while others do not. There is no discussion of why some patients respond so positively while others do not.
I personally hope that more research will be done to isolate the difference among different patients to help find a way to help all patients. I would also love to see if there are other ways to increase BDNF in the brains of PD patients using other techiques. Could it be possible that this particular protein could help increase the quality of life for PD patients for numerous years? Could the brain help repair itself if the neuronal death is slowed or stopped? I am of the opinion that further research into these areas and questions is needed and needed soon.
To read one article about this study please click the link below.
http://www.sciencedaily.com/releases/2008/09/080902171151.htm
The study does note that not all patients seem to have the same results from DBS. Some patients have a marked decrease in symptoms and a slower progression while others do not. There is no discussion of why some patients respond so positively while others do not.
I personally hope that more research will be done to isolate the difference among different patients to help find a way to help all patients. I would also love to see if there are other ways to increase BDNF in the brains of PD patients using other techiques. Could it be possible that this particular protein could help increase the quality of life for PD patients for numerous years? Could the brain help repair itself if the neuronal death is slowed or stopped? I am of the opinion that further research into these areas and questions is needed and needed soon.
To read one article about this study please click the link below.
http://www.sciencedaily.com/releases/2008/09/080902171151.htm
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