I am delighted to announce that our next zoom session will be taking place at 7.30 pm London time on Monday, the 21st of February.
Dr. Jonathan Sackner-Bernstein will be talking to us about: "What If I Discovered the Silver Bullet?"
Motivated by a friend’s suffering from Parkinson’s, Dr. Sackner-Bernstein focused on a gap in our understanding of the disease: no one had so far measured the amount of dopamine in the dopaminergic neurons of people with Parkinson’s. This is critically important because dopamine is toxic to these cells, which would then be a driver of neuron dysfunction and death, leading to disease progression.
He published his analysis last summer in the Journal of Parkinson’s disease showing that these critical neurons do not lack dopamine – they have excess dopamine. This led him to design a clinical trial to test a drug that addresses this newly defined mechanism of disease.
Please see the following article for more information:
Dr. Jonathan Sackner-Bernstein was a renowned clinical trialist in cardiology before leaving academics to pursue medical product development, including drug, device and biologic therapeutics.
He served as associate director of the FDA’s device center, where he led diverse programs highlighted by the White House’s first Entrepreneurs-in-Residence program, the Center’s innovation initiative that led to the Breakthrough Devices program and a collaboration between FDA and DARPA to develop systems and products for the Medical Countermeasures Program (focused on responses to chemical, biologic and radiologic mass casualty events).
After serving at the FDA, Jonathan consulted for DARPA, with responsibilities including regulatory strategy and commercial transition of their programs/projects. Jonathan supported the launch of DARPA’s Biological Technologies Office, with a primary focus on neuroscience and big data programs.
Jonathan’s academic experience ranges from First-in-Human to international trials, as a clinical investigator and trial leader. Sackner-Bernstein held academic appointments in cardiology at Columbia University and North Shore LIJ Health System (Northwell) following training at Mount Sinai Medical Center. He earned his undergraduate degree in electrical engineering at the University of Pennsylvania.
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Michel0220
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I just looked him up. A YouTube video from 6 years ago he prescribed statins. I wonder if he has updated his thinking since then. If he has not, you should reconsider listening to him on any other subject.
That is a legitimate concern. I did not see the video you are referring to, but it I did find the following, which I think puts those concerns to rest.
Dietary Intervention for Overweight and Obese Adults: Comparison of Low-Carbohydrate and Low-Fat Diets. A Meta-Analysis
"These results suggest that future evaluations of dietary guidelines should consider low carbohydrate diets as effective and safe intervention for weight management in the overweight and obese, although long-term effects require further investigation."
2 silver bullets in consecutive weeks. You're going to have to think about rebranding
Some observations
Designing a clinical trial is not the same as implementing or completing one. When will the trial report?
"The study's findings explain why treatments to increase dopamine don't slow or reverse disease progression". So who thought they did? Nobody in the medical or scientific world has ever claimed dopamine supplementation slow or reverse the disease, nor had any expectation that they would. Magicians refer to this as misdirection
CONFLICT OF INTEREST
Jonathan Sackner-Bernstein is sole inventor on a patent filing for use of tyrosine hydroxylase inhibitors as therapy for Parkinson’s disease.
Emh! WTP, you could sign up and explain your point of view directly to him and compare your experience with his, then you can bring him back to us.So we will all have more understanding without commenting on your cherry-picking on presentation articles. It's free.
Has there been some progress since the last zoom meet with Sackner-Bernstein (8 months ago), or is this the continuation of the ongoing promo? healthunlocked.com/cure-par...
It is an interesting topic and will certainly raise questions and support from both sides of the topic.
An excellent opportunity as @GioCas says to simply ask the questions directly to him and listen for yourself.
We have the benefit on HU of some very wise and sharp minds concerning PD so I think it would help us all to hear some of these questions and answers live when the speaker is under a little scrutiny so please do join in, or if it's inconvenient then perhaps send in questions
I urge all who can to attend this incredibly important talk. His reputation is amazing and he will have some very surprising and shocking things to say that are crucial to our health as Parkinsons patients.
Do the "dead" neurons stay in the brain or are expelled by the body? What happens to them? As Dr. Bergman suggests they hibernate and with the right manipulation become active again? Food for thought. . .
Despe, look up senolytics. It’s fascinating. Quercitin and Ficetin are both senolytics but a new and in some respects better one is coming derived from grapes, it is from grape seed extract, PC1 I think. Senolytics help clear out the dead and dying cells which damage the adjacent cells. You research do much that I might be sharing nothing new!
Will do, matcha. How about eating grapes swallowing the seeds, which I have been doing instead of spitting them out ? Quercetin has been permanent on our supplement list.
Although I too prefer to start with diet, I think those grape seeds are going right through you like they do little birdies who deposit the seeds all over. ☺️ I miss my old name but it won’t let me use it again. Boohoo.
One question arises spontaneously: but if the dopamine neurons are dead and removed, at the autopsy the brain tissues in question should not be spongy as in other brain diseases where the cells die and are eliminated and I quote: "SIGNS AND SYMPTOMS … When brain tissue from a person with Creutzfeldt–Jakob disease (CJD) is examined under a microscope, many tiny holes can be seen where the nerve cells have died… ".
Oh! sorry. I just wanted to say that at the autopsy perhaps one could determine whether the dopamine cells are hibernating or dead and digested based on the texture of the tissues like Creutzfeldt – Jakob disease. see chapter signs and symptoms of Creutzfeldt – Jakob disease Wikipedia
To the best of my knowledge this has not been done and I see no reason as to why other than that they are not incentivized to find the root cause. Why learn how the holes in the boat start when we can be prescribed meds that enable us to stay afloat despite the holes. Or meds can be made to bale out the water. I would prefer to not be a sinking boat in the first place. I’m presently endeavoring to learn more about autophagy, apoptosis, and senolytics to better understand this.
PD brain is probably not full of holes aka dead neurons.
'Importantly, the existence of dormant neurons was observed in the brains of human patients. Analysis of postmortem brains of individuals with mild and severe Parkinson’s had a significant population of dormant neurons surrounded by numerous GABA-producing astrocytes....The fact that inhibition of dopaminergic neurons by surrounding astrocytes is one of the core causes of Parkinson’s should be a “drastic turning point” in understanding and treating not only Parkinson’s but also other neurodegenerative diseases"
Could these “dormant neurons” be due to a proliferation of senescent cells? And the over abundance of senescent cells could be at least in part due to the ROS resulting from inflammation? Just a newby research nerd hopeful guess. If this theory holds then reducing inflammation and engaging senolytics could help?
Not quite. Read more detailed explanation on the below SOP article for the dormant "inactive" neurons in relationship to GABA and reduced TH.scienceofparkinsons.com/202...
No matter, it is clear there's no silver bullet. True healing could only happen through a multifactorial approach, and yes addressing inflammation and restoring cellular health are definitely part of addressing the root "causes."
Thank you. I will definitely read everything you sent. When time does not allow me to read, I seek videos. GABA is taken as a supplement for relaxation and sleep. How very bizarre. It has a relaxing effect. Thank you for the info. “GABA has a relaxing effect on neurons in the brain.”
Yes, GABA is an inhibitory neurotransmitter that allows for relaxation and sleep. It's ultimately all about proper balance, just as in most other things.
Not in this context. It'll pay to digest the SOP article. It gives credence to the documented PD reversal cases, which basically means reviving the dormant TH-negative, but AADC-positive neuromelanin cells, restoring the ability to regenerate dopamine, especially in milder cases where trophic support, regenerative interventions, and addressing the culprits that led to astrocytic reactivity could actually make a huge difference.
Husband took Azilect for a short time, but it caused him a lot of confusion. He had to stop it. Scientists are still debating whether MAO-B inhibitors slow down PD progression.
This is very interesting (plus a lot more on senolytics).
Yes it is a hot debate, and pharmaceutical MAO-B inhibitors such as Azilect may only help for a short duration. The use of MAO-B inhibitor obviously does not address the root causes that gave rise to the pathological conditions that engendered ruthless astrocytic behavior.
Why would the MAO-B inhibitor only help for a short period? The Korean trial used Selegiline and not Azilect. I wonder why. Selegiline is an MAO-I I thought? It’s used for depression too. And can be prescribed as a transdermal patch. I’m interested in it to avoid continuing to inundate my gut. Rescue-ma, do you think the natural MAO-B inhibitors could be as effective as Azilect? Quercetin, turmeric, EGCG, etc all have so many other benefits.
They only work for a short period with diminishing effects observed in long-term treatments because the irreversible MAO-B inhibitors such as Selegiline and Azilect bind covalently for eventual enzyme degradation.While helpful, natural MAOIs are probably not specific enough for stopping the aberrant astrocytic GABA excess for significant therapeutic effect.
As far as the drug route, I'm hopeful for the reversible MAO-B inhibitor such as KDS2010.
Are you familiar with glutamates effect on ALS and PD? As I was learning about GABA, glutamate came up since it precedes GABA. I’m just beginning to learn this but my current understanding is that increased glutamine is associated with PD which makes sense since increased GABA is. L-serine, amino acid, has been researched for this and is being researched for ALS. Do you think looking in to means of reducing glutamate could be beneficial? It was researched quite a bit but stopped. Now it’s being trialed for ALS
Imbalance and abnormal homeostasis is the outcome of various underlying holistic culprits. It's important not to stress on any one particular subject myopically - try to leave this to the scientists/researchers than getting trapped in the rabbit hole.
No no dear Despe! GABA is a very important neuro-transmitter but in PD patients, there is a more than typical amount (I posted a human trial on this) The excessive GABA surrounds the dopamine neurons and it is hypothesized causes them to go dormant. I therefore hypothesize that decreasing GABA might be beneficial.
Instead of holes there are clumps of beta-amyloid plaques that have choked the life out of the cells. Whether the cells are there in a dormant state or not, should be the question. Gioc
I don't know if any of you were viewing the event but it got hacked so I had to go off and now I am wondering if we have to worry about these hackers having access to our computers?
Not at the moment but encouraging signs as JSBs presentation led to some additional funding discussions. I plan to ask him for an update after the summer.
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