From James Beck, Ph.D., Director of Research ProgramsUnderstanding how Parkinson’s disease starts and how it progresses remain two of the key unanswered questions about the disease. This is why a recent story in the New York Times caught my eye.
The article described how two independent groups of scientists found evidence that Alzheimer’s disease may spread from brain cell to brain cell much like a virus. These scientists engineered mice to make a human form of a protein called tau in only one small part of the brain. Clumps of the tau protein are a hallmark of Alzheimer’s disease. Like the rubble of demolished buildings, these clumps are all that are left of brains cells that have slowly died because of Alzheimer’s.
Proteins and Clumps
Proteins in the body are folded into special shapes … almost like pieces of origami. Some proteins, if they are not folded correctly to begin with or become “crumpled” due to some cellular problem, will stick together in clumps. Similar to how clumps of the protein tau are a hallmark of Alzheimer’s, clumps of a protein called alpha-synuclein are the hallmark by which Parkinson’s disease is diagnosed. These alpha-synuclein clumps are called Lewy bodies.
Parkinson’s and the Contagion Theory
Parkinson’s researchers have long noted what appears to be the spread of Lewy bodies from one brain region to another. Researchers observed possible clinical evidence that Parkinson’s could “spread” from one cell to another, when fetal cells were transplanted into the brains of people with Parkinson’s disease. The transplants subsequently developed Lewy bodies. That is, something about a Parkinson’s brain made genetically unrelated cells that were only a few years old develop the signs of Parkinson’s disease.
What came out of these observations was the controversial idea that Parkinson’s, once started, might be transmissible from brain cell to brain cell.
Several recent scientific papers are beginning to lend credence to this idea:
- Last year, Dr. Patrik Brundin’s research team in Lund, Sweden published a paper demonstrating that mis-folded alpha-synuclein (the basis of Lewy bodies) can spread from cell to cell in culture and could also spread in the brain of a mouse.
- More recently, Dr. Virginia Lee's team from the University of Pennsylvania published similar findings this past November.
- At a recent New York Academy of Sciences meeting on Parkinson’s disease, unpublished data was presented that also demonstrated how a single injection of alpha-synuclein clumps into a mouse brain could lead to the widespread formation of Lewy bodies in many different parts of the brain.
What Does It Mean?
Well it brings hope that a Parkinson’s therapy might be found in one of two ways: using special antibodies that target alpha-synuclein or a vaccine which primes the immune system to also target alpha-synuclein.
Either approach may not only halt the spread of Parkinson’s disease but maybe could also prevent it.
Your Feedback
What do you think about the recent Alzheimer’s study and how it relates to Parkinson’s? As always, please share your comments and I will do my best to respond.
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16 comments:
WOW - that is great news. If it can be proven for sure and if they can find a way to reverse things - I would equate it to almost a miracle. I would mind being a guinea pig for something like that. If you happen to hear of any ideas as to how to make that happen, I'd be interested. Thank you for that good news.
I think this is a very exciting thing to follow. I would like to see some human tests. This could lead to a prevention of Alzheimers and Parkinsons. I just had DBS and it has done wonders to delay parkinsons, but we need to continue the researsh to stop parkinsons.
This seems like breakthrough news. How long will it be before this is confirmed in PD/DLB patients and potential treatments developed? I am not sure how much time we have left.
As founder of an active Parkinson Support group, I am anxious to report these findings at our next meeting. This will give hope to our members and their caregivers.I know there will eventually be a cure, but the sooner the better. Thank you for sharing these articles.
Does this mean a stop to a current level of disease, or does it mean a reversal of the disease process? these are different outcomes>>>
After my husband, diagnosed with PD for 12 years but still not on PD meds showed continued mild memory problems and then rather sudden examples of illogical thinking, he was put on Aricept. He is on multiple drugs for heart and lung problems. From what I read, the Exelon patch ( the only Alz. drug approved for PD dementia) would be a better choice. Should I be "nervy" and ask the neurologist about it? (I doubt that he'll think much of being 2nd guessed, but I'm willing.)
This would appear to be very promising information. OK, so we develop a vaccine; it works. No more PD. But wait, what about those of us who already have it, "progressing" along to our miserable demise in falls and dementia. Is anybody working on how to reverse it; or at least stop it in its tracks? Or must we shut up and be content with semi-functional symptomatic treatment and drugs which each help but interact badly.
Great to see so many comments. A couple themes that are being raised.
• Timeline: For both PD and AD, this is very early stage research. Unfortunately, it does take time to translate these findings into something we can see in the clinic. (However, that is useful time as it can help weed out the unsuccessful ideas!)
• Treating or Stopping PD: If the theory holds that PD is progressing in part due to the spread of mis-folded alpha-synuclein, then treatments that help the body to rid itself of synuclein are likely to really put the brakes on the advancement of PD. It won't be a cure, as there is likely another reason why PD gets started in the first place; but it could make a real difference by making a PD a chronic disease instead of a progressive disease.
What might this mean to those who already have had PD for a while? Best case would be that it could help restore function to neurons that are no longer able to work and are dying...much like water to plant that is dying in a drought. It won't recover what is lost, but evidence suggests that the neurons lose function first before dying...and that is where the symptoms of PD arise. Worst case, would be that this approach is of no help. Bottom line is that this remains the realm of speculation and we are all hopeful the science moves quickly.
To @Anonymous with the husband with PD for 12 yrs, I think that there is nothing wrong being an advocate for your loved ones. You should feel free to ask the neurologist about different treatments that might help your husband. Good luck.
I should add that whenever you have specific questions about your own PD or that of a loved one, a call to PDF's excellent help line would a good start. The number to PDF's Parkinson's Information Network (PINS) line is: 1-800-457-6676.
I want to be sure that I am understanding the article correctly. PD can be transmitted from brain cell to brain cell. So the cure would be to create antibodies that would target cells with PD or a vaccine that would destroy any PD cells that might form. I could see where this could lead to a cure for even advanced PD. If you could destroy the brain cells that had PD and replace them with brain cells without PD by using stem cells.
No effective treatments has been invented yet to cure Alzheimer's and Parkinson's disease other than prolonged medication for lifetime. I shall like to know about effective treatment of these 2 diseases from this blog.
In response to the request to clarify how the antibodies might work, let me see if I can provide a straightforward explanation. For Parkinson's, the antibodies will target the alpha-synuclein protein I discussed in the blog post that gets released from damaged and dying cells--the brain cells are untouched.
Another way to think of it is that these cells are like a red shirt in a washing load of white clothes...the color (alpha-synuclein) will bleed and turn everything pink. The antibodies act like those new color catcher sheets. They sop up the loose red dye and prevent the rest of the laundry or, in this case, brain cells from getting contaminated. The red shirt and brain cells are left untouched in the process. So the antibodies may not cure the disease but they may help slow it down significantly.
To @Retirement Home, you can rest assured as we learn about new scientific advances we will be covering them here as well as the Science News section of the PDF website.
Thanks to all for their great comments!
So glad to read this as I am new to the information regarding PD. My father was just diagnosed. I feel there is hope now.
My fathers mother had AD. She lived close to 18+yrs. With it. At first, my 74 yr old dad seemed so out there, that we thought he may have AD. Docs in phila say its not AD..its PD. Besides tremors, how can u tell the differences between the two?
My Parents have 7 children all mature adults now, but 1 girl has Alzhiemers diagnosed about 2 yrs ago at age 77 the other girl has Parkinson's dx 7 yrs ago at the age of 76. Do you think there is any correlation that exists. My belief is that we all have mutations or genetics that we have that differ in a family but certain ones increase and are passed down and certain ones have the disposition to getting the disease. In this case because the 2diseases are so much alike in many ways we have 2 people with the bad genetics for what ever reason timing or a couple different genes thus the two diseases. I am intersted what you will think and why. Thank for listening.
This is very good news, even if it comes to fruition too late to help me personally. Regardless of whether this research leads to an actual treatment or not, it will most certainly help in the quest for a cure. The most significant thing that PD has taken from me is my future; I always thought that I would be one of those sassy, active old ladies that seem so much younger than their years. PD has destroyed that vision. When I hear of research like this, I feel hope that my future might be returned to me; I might yet become that sassy old lady!
@Mary Damico - Since I am not a clinician, I want to avoid getting into details how to differentiate a diagnosis of AD vs. PD. Nevertheless, as you indicated, PD has several cardinal features that help with the diagnosis, including tremor at rest, bradykinesia or slowness of movement, rigidity or stiffness that is felt by a clinician, as well as balance and gait (walking) problems. If you would like a second opinion, I would encourage you to call our Parkinson's Information Helpline and someone could provide the names of several physicians who are trained in treating people with Parkinon's disease.
@Anonymous - I think you have a very good question that goes to the heart of the matter - what causes AD or PD? For most people we do not know. However genes are certainly part of it, in the sense they are not the cause but contribute to the problem. Environment is likely another contributor but not the cause. As you can imagine, knowing the cause is a topic of continued and intense study.
@Marian Bumala - PD or not, I hope you become that sassy old lady! You are right, there is hope. It may not be today, but our ambition is that it will be soon.
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