lewy bodies develop eventually on cell wall like a battery plates phosphate up when not functioning
, explains unreliability of cell grafts and transplants, which don't last because the inactive non functioning cells " must be removed, like a dudd battery left connected in your car would inhibit new battery UNTIL THAT NEEDS RECHARGED
PARKINSONS CAN BE SORTED BUT RESEARCH NEEDS ORGANISED
DOPAMINE IS ONE OF 3 NEUROTRANSMITTERS INOUR SYSTEM THEY ALL WORK TOGETHER DOPAMINE IS PERHAPS NOT ALWAYS GUILTY
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There's more than 3, The following is taken from wikiperdia
Types of neurotransmitters[edit]
There are many different ways to classify neurotransmitters. Dividing them into amino acids, peptides, and monoamines is sufficient for some classification purposes.
Others: acetylcholine (ACh), adenosine, anandamide, nitric oxide, etc.
In addition, over 50 neuroactive peptides have been found, and new ones are discovered regularly. Many of these are "co-released" along with a small-molecule transmitter, but in some cases a peptide is the primary transmitter at a synapse. β-endorphin is a relatively well known example of a peptide neurotransmitter; it engages in highly specific interactions with opioid receptors in the central nervous system.
Single ions, such as synaptically released zinc, are also considered neurotransmitters by some,[7] as are some gaseous molecules such as nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO).[8] Because they are not packaged into vesicles they are not classical neurotransmitters by the strictest definition, however they have all been shown experimentally to be released by presynaptic terminals in an activity-dependent way.
By far the most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain.[3] The next most prevalent is GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate. Even though other transmitters are used in far fewer synapses, they may be very important functionally—the great majority of psychoactive drugs exert their effects by altering the actions of some neurotransmitter systems, often acting through transmitters other than glutamate or GABA. Addictive drugs such as cocaine and amphetamine exert their effects primarily on the dopamine system. The addictive opiate drugs exert their effects primarily as functional analogs of opioid peptides, which, in turn, regulate dopamine levels.
We practically have to become doctors to learn how to understand the care we are offered and make the best decisions for ourselves. But at educational programs, often doctors are surprised by how up-to-date and informed patients and advocates can be even of research findings that came out that week. It's like a full time job/work expands to fit available time--at least for me (caregiver).
The more we learn, the more we realise that we know nothing. Should I give up trying or just go with the flow. I am overwhelmed with the amount of infromation that comes our way!
In answer to your question John, the answer is NO! Take yourself as an example, if you had given up many years ago you would not have bothered to try and succeed to reverse some of your symptoms. Giving up means no progress.
I don't wish to be offensive but I think this thread typifies our level of knowledge of PD. "Our" being the people who suffer the effects of PD, the patient and caregivers. The Prof's original post on this thread is ignored, apart from a cut and paste from Wikipeda.
Sure we are "experts" on living or trying to live with the symptoms. But when it comes to understanding PD, the vast majority of us would fail to surprise doctors with our up-to-date knowledge. I'd guess if you asked a random 100 patients to explain in simple terms what PD is, not the symptoms but the actual disease, you would be lucky to get a correct answer.
JohnPepper says, "The more we learn, the more we realise that we know nothing." Change the last word to "so little" and I'll agree with you.
I was being phylosophical. I think I know a fair amount about Pd, but in the larger scheme of things, I know "so little". I have this terrible suspicion that the 'powers that be' do not want to find the cause or a cure for Pd, because it would kill the goose that lays the golden egg. You can imagine just how much money is generated by people with Parkinson's disease? It is enormous and ongoing. As I have said in other blogs, I feel sure that GDNF is the cure we are looking for. It has been shown to repair damaged brain cells and is produced, naturally, by the brain, when we do certain types of exercise. If this is correct, and according to the paper delivered back in 2006 at the first World Parkinson's Congress held in Washington DC, it definitely is so, then why are our neurologists not telling every single patient that he/she must start to exercise regularly? Why had Amgen produced an artificial GDNF - which was very successfully tested in 1993 - disappeared from view? If we know of something that reverses Pd, then why have we not been concentrating on it? Hence my skepticism!
I used to believe in that conspiracy theory, there's more profit to be had from ongoing treatment than cure hence drug companies shelve the cure. If you believe a cure is a one off event then the profit motive is there. But if the cure is continuous treatment, then the pharma industry wins either way.
Modern investors have very short term views which force companies to produce optimistic forecasts and follow up with profitable results otherwise computers start dumping shares wiping billions off the balance sheet. I feel if they have a miracle cure they would pursue it rather than shelve it.
As for GDNF, I share your optimism despite a recent setback when the oral version, Cogane, was abandoned when in clinical trial it was found to be no more effective than placebo.
My understanding of the Amgen project is that the method of transporting it to the brain was the problem rather than the drug itself. The fluid carrying the drug down the tube to the Basal Ganglia worked well and produced remarkable results, not only did it deliver a dramatic slow down in cell loss as hoped for, it regenerated cells thought to be dead. Alas though the fluid leaked back up the outside of the tube and was delivering GDNF to other parts of the brain, hence the project was deemed unsafe.
Bristol University in England are however carrying on research and have modified the delivery method. Last year they were seeking funding for clinical trials so as far as I understand, GDNF research is steaming ahead. Just hope it comes soon, in time to save my my degenerating brain!
Yes! As a retired businessman, I understand full well the need to make profits. However! I have to ask myself, is 20 years a reasonable time taken to improve the delivery of GDNF or is someone dragging their heels? We know that GDNF is a winner, and the only drawback is finding a way to deliver it to the correct area of the brain, then why not pump everything into getting it done? The record shows that it took another ten years to do further tests! Come on! Give me a break! If they can draw this out for fifty years, think of all the money they continue to make! How many cures for any health problem have come onto the market over the past fifty years? I rest my case. Nobody in their right mind, running a pharmaceutical company would be spending billions on looking for a cure for anything. It would inevitably lead to a reduced market for the traditional remedies.
Hi Professor. I wish I could afford to pay for a drug trial, but I don't think that it would further the cause. Someone would come along and buy the patent and it would just disappear from sight. You and I atre not in the position to manufacture and market the GDNF!
Just saw a Tampa doctor on local TV news discussing the serious sometimes fatal problem of antibiotic resistant bacteria in hospitals. He stated they are beginning a private project for their development (not sure where or funding) of such an antibiotic because pharmaceutical companies will not as profits would be too low.
if it is the miracle cure they talk about as you said throw everything into it . After all if it works look at the new they would save in keeping people out of hospitals and nor sing home , ambulance call out OTs and Physios . benefits .
But most of all getting our families back and having more equality of life .
Too true they are bigger than us, but we Parkies hold a golden key - they need us for three of the four stages of clinical trials. Recruiting for trials is notoriously difficult and costly.
In my humble opinion, the most effective way forward for a Parkie group is to focus on helping in that area. But we need to work with the industry, not oppose it. And we need to tow the ethical line. Bluntly we have to grow up and bury the conspiracy theories. Accept that pharma companies are big business, have shareholders, must make profits to reward shareholders etc. And above all realise our future is in their hands. A similar argument for academic research.
We could influence the direction research takes in a positive manner by offering support to projects we are interested in.
Hi Grey. For the past ten years I have been trying to tell the world that I have been able to overcome most of my Pd symptoms, as a result of doing lots of walking and of managing my stress levels properly. I gave up my job, at great expense to myself, and concentrated on my health. My major advantage I had over others was that I did not get involved in taking LDopa medication. It is my feeling that once we start taking the LDopa, we become trapped in it. The side effects become more problematic than the Pd. If we stop taking it, we cannot function properly, so we have to take more of it to stay functioning at all.
I'm so glad the penny has dropped re our (PwP) relationships with drug companies. So much energy has been wasted in opposition, so much brain power on pursuing conspiracy theories - welcome to the world of grown ups!!
We can indeed influence the direction research takes by supporting projects at every level but best of all...VOLUNTEER.
John, I share your frustration, not only with GDNF. As far as I'm aware, it takes on average 13 years from identifying a useful molecule to grant of licence. 10 years minimum. As the trials on humans began early in the last decade and have suffered major setbacks, the time-scale is not exceptional.
13 years, however, is too too long for people with a progressive disease but maybe that warrants a new thread. In fact it's so important to us, a new forum across progressive diseases, dedicated to reducing this period should be started.
If I knew for certain who makes the rules and if those rules are reasonable to all concerned, and those rules are not there to maintain the status quo, for as long as possible, then I would be much happier. I have to reiterate my question: "How many CURES have ben found for ANY health problem over the last fifty years?" If the answer is zero, or very few then, either the scientists are wasting their time, or someone is effectively stopping these cures from reaching the marketplace. If we all think about this situation, we must soon realize that there is something terribly wrong going on.
I am a little more optimistic about 'the powers that be'. Whatever the motive of pharma i just cant imagine that they are some how ensuring that scientists and physicians will not find a cure. Pharma is profit driven and they can certainly put obstacles in the way but many many good people are working hard on our behalf, they want us well.
Thanks Hikoi. I watched the latest video on DR Stephen Gill's latest news on Sky News this weekend. I am fully aware that this project is bumping along the ground at a leasurely pace, but knowing that this is the 'cure' we are looking for, is everybody doing their best to bring it to the market?
I wish i was that certain that this is THE cure. I do think it will be a life changing treatment for some.
GDNF was first identified in 1993. The first human trial was 2003. It wasnt until 1997 that the first genetic mutation in Parkinsons was identified. We still have much to learn I believe and i dont think one 'cure' will fit all.
Many differing types of PD are now being recognized and as with cancer, i think the treatment will eventually be tailored to each person's disease.
I don't believe GDNF is a cure, but a treatment. Much closer to the cause and less of a symptom basher. But as far as I understand it requires continuous treatment for life.
Because of the variety of patient symptoms, PD is often suspected of being several diseases, currently diagnosed as one (well idiopathic variety is). One size won't fit all is a real fear.
Hi Hikoi. To the best of my knowledge, Dr Stephen Gill carried out his first trial of GDNF in 1993. I might be wrong, so forgive me. In 2003, two further trials were carried out, unsucessfully in the USA, which prompted the manufacturers of the GDNF (Amgen) to stop the production of GDNF. I ask you: If the first trial in 1993 was so successful, how could the next trials, ten years later, have proved so unsuccessful?
Hi Hikoi. To the best of my knowledge the trials were carried out in Frenchay hospital in Bristol, England on seven Pd patients. All seven recorded very successful results and one died of unrelated causes, but his autopsy revealed a very positive proof that new Glial cells had developed and existing cells had been repaired. Have you looked into this?
There are indeed extremely good basic researchers and doctors out there as well as others pushing in the right direction. I've worked in basic medical research (CDC) and the intensity of "I must know the answer to this question" is there. It's all about leadership, funding and getting a group going on a project.
Shortly thereafter Amgen demands removal of the installed infusion devices and cancels the study citing: a) no measurable difference between test groups and control groups at 6 months, and b) the discovery of GDNF-induced “lesions” on the brains of test primates, particularly the cerebellum and thus declares GDNF “unsafe.” c) They also cite theoretical concerns that as a peptide, GDNF could initiate an immune response against itself and in addition, the body’s own natural GDNF, eventually making all forms of GDNF ineffective in patients
I agree with much of what you write except the reason for so little response to the Profs post. Perhaps others were like me. I couldn't grasp the point being made from lewy bodies to cell grafts to neurotransmitters.
this is my own theory. it may not be wholly correct, but read it
cell grafts fail to last or generate unstable control seen as diskinesea
, because like in a car a dudd battery( cell)left connected, would render ineffective any replacement, eventually.(in performance terms)start car not start car, sometimes maybe
if...the cells dead(non functional) gobbed up with transporter protein clumps cant be recovered they. need to be removed, such that its " brand new balls" re instating dopamine quantity/ quality ensuring reliable result,(and not , if we leave the old cells in whack in new cells, I think
its not gonna produce results we must get, its a piss in the wind,
It is hard for me to understand you professor, but from what I do understand about not getting rid of the alpha synuclien, the cells must be got rid of. I leave all that to the scientists, I have nothing to suggest to them about cell death and replacement.
so what follows is.original AMPLIFIES the spaces in my first post.
and is fuck all too do with pete-1 lesson in brain chemistry. THE EXPLANATION
My investigations provided edvidence dopaminergenic neurons will still fire even with no dopamine , FIRE but fires blanks, L-DOPA created in gut,.competes with other amino acids for transporter proteins,that TRANSPORT to many parts of the body as well as brain. ldopa gets a free ride to the brain , where its converted to dopamine.. , only once and that occurs in SLEEP.the ability of the brain to store dopamine in the main, detemined by sleep. reduced or low levels of dopamine goes undetected until a resulting surplus of transporter protein has to be dumped , over a period forms protein dodds/clumps on cell wall , , no cell deathOR NON FUCTION is reported , the cell fires blanks only reduced movement control results motor control reduced to coarse only is typical first indication...........as that pesky wabbit says"THATS ALL FOLKS
Obviously you can not go on like this, so why not consider asking your Dr for a prescription for Amitriptyline. It's actual use is for depression at much higher doses than you need it for sleep. Many people have used it as a sleep aid; it comes in units of 10 and 25mg, you might start off with a 10mg tablet nightly, going up to 30mg at most. Many people take much higher doses than this for depression. It's worthwhile researching to decide whether to go for it.
Thanks, I've not tried this in years but maybe it would help. I've decided to try exercise especially outdoors first and see if it might help reset my wake/sorta sleep cycle. But I'll keep it in mind. I appreciate you telling me...
hiho silver away. PART DEUX. HOPE YUR NOT SLEEPIN..parky tefalheads out there that's you grey, hikoi to name 2 who are well informed
.ropinerole or pramipexole were the favoured replacement for pergolide( GOT WITHDRAWN) D/ AGONISTS but responding with different Dreceptors I HAVE BEEN TAKING ROPINEROLE ,GIVES A LITTLE RELIEF PRAMIPXOLE DID NOTHING THE ROPINEROLE HAVE SWALLIED long time and now needed to supplement with Ldopa, but LDOPA MADE ME WORSE STIFF (IN THE WRONG PLACES ) CRAMP UP came off it,
actually getting a diagnoisis takes a lot of luck if your a parky and as we say in bonny Scotland most doctors are text book players, somethin not look- uppable ,theyHIVNAY GORRA SCOOBY
( scooby doo ..clue)so ropinerole works ..ish LDOPA NOT so,,,, ,CONCLUDED my symptoms are not dopamine derived
the dopamine agonists don't only respond with d receptor, a 5H-T group receptor get a lesser HIT WAS ALSO LISTED
5- HT group IS SERETONIN another neurotransmitter ( steady pete) 3neurotransmitters work together in dopamine system
10 symptom boxes serotonin deficieny, I tick every one HOPEFULLY BETTER RELIEF FOR ME
there are many neurotransmitters the system more complicated than catchin a haggis
meds you take are decided by your doctor . RELIEF CAN TAKE A WHILE TO FIND NEVER GIVE UP........ THIS FORUM IS VERY HELPFULL HONEST AND CAN PROVIDE HOPE
I caught a haggis once. I won't say exactly how, but beyond just skill and uncommon luck, and despite the intimidating presence of PETH (People for the Ethical Treatment of Haggis), it did involve an outrageously expensive bottle. Having summarily consumed the entire bait, he then told me the history of his species. For this amazing disclosure (telepathic, it was), I honored the haggis' request for no photos and let him go. I excitedly passed on this priceless information to the local New World Celts group.To their shame, the NWC group did not believe me, offending me so that I have never again hunted the haggis for them.
Most of all that you say goes over my head but I can sort of get the Gist of it ..
My husband at the age of 80 has only been given Sinemet along with the Neuro patch . I cannot say that it has ever been particularly helpful and he has slowly got worse . It has always been difficult for him to explain how he feels , this is a man who had been very expressive .
Whenever I told the consultant that like some people say they can see a difference after taking their medication we never have done . He said it was like that for some people .
The new treatment if it ever comes to fruition will be far too late for us and so many others .
It is difficult to know, at the age of 80, whether deterioration is the result of aging or Pd. I turn 80 next year. but no two people are alike. I still am very active, but I know that my fitness is deteriorating, slowly. But what do I expect? I do know that, "WE only get out what we put in". That goes for everything in life. I am a firm beliver that if a medication does not do the trick within a reasonable amount of time. then STOP TAKING IT!. Exercise is still the best approach to dealing with PD.
Stiffness /rigidly no petrol in the tank to move , coordination , goes off like a light switching off . Poor concentration all gets too much . Almost like being locked in .
Of course with no mobility he has lost most of his strength . He is using his arms and not his legs . once he is out of bed he can only get out of the chair when he uses the commode . Cannot get him into the toilet even . We have brought the bed downstairs .
The GP we used and was so supportive has moved , he was quite upset at my last visit to him because he realised how much I would miss being able to talk to him . Our consultant retired last Christmas and I haven't that much faith in the caretaker Dr . they are advertising for a new one . That's if they have enough Money !!!!
H started on the lowest dose and went up to Sinemet Plus x 3/4 daily with the CR at night Dropped it down to 110 because I thought he seemed worse after taking them but is just the same . Might have even needed the higher . It's a minefield . He was getting some nightmares not happening now but I think the consultant worries about him be ing sensitive /reactions to meds . Took Digoxin for the heart once and that was horrendous . Soon stopped those . Anything is worth trying I think after all it is trial and error as long as it doesn't kill you .
THE PATCH , THIS A DOPAMINE AGONIST BUT THERE ARE MORE THAN 1 AGONIST, THERE ARE MANY NEURO TRANSMITTERS, ALL WORKING TOGERTHER IF THERE IS A DEFICINCY OF ANY, THEN MOVEMENT CAN BE AFFECTED , AN AGONIST AMPLIFIES EMULATES THE SHORTAGE
DIET IS A BIG PLAYER TRY STAYING OFF FOODS HI IN PROTEIN. TAKE MEDS HALF AN HOUR BEFORE FOOD AVOID FOODS HI IN PROTEIN THE EVENING SLEEP IS NOW REALISED TO BE VERY IMPORTANT MAKE SURE IT HAPPENS
AGONISTS TO ASK YOUR DOCTOR FOR,PRAMIPXOLE ROPINEROL
THERE IS AN LDOPA INJECTION THIS MAY BE YOUR BEST SHOT IF THE AGONITS CANT GET YOU A SCORE
DONT GIVE UP LOOKING,THERE IS ALWAYS ANOTHER OPTION
We have been aware of the Protein , I leave it until at least an hOur before taking th Sinemet and an hour after eating .
He is sleeping at night although not always as comfortable as we would like and on a good day get him to raise his legs and have a nap even if for half an hour .
I have his Sinemet 110 at 8 this morning , so I thought I would try by giving him a Half of Sinemet 250 cR at 11 am , I have given th second half now at 3 pm .
I have felt he isn't even enough , was going to ask about the duo dopa . Not sure if that is the right way to spell it .
He gets a sore bottom and pain in his left buttock , now trying by placing something under his right foot to raise his knee it a little . working at the moment . I am not giving in to this dam thing . Although it might give me up lol.
I need to get him in a better place before I can get him to see anyone .
you are doing all you, can to support your hubby, no one would expect you have to live his life 24-7,you must have some relief to have a life of your own , I would say
arrangements made ensuring his wellbeing the care support to help manage things are as good as . can be
in my experience Parkinson nurses know more about what works than most consultants who look it up in a book..
..incidently has anything he has been given everv worked, how long has he been bad?....
I have had a social worker , OT etc very helpful, now having two carers morning and night . I only need them for getting him I and out of bed I want to do the test myself But they have it all in the plan so are very aware . The district nurse is at the end of the phone .
They are things that I have arrange myself , only advice I have had really is from Googling and talking to other like yourself .
I like to think I can help others who are starting this journey and make it easier for them than we had .
The carers cannot be here all the time to,me can they . I know I can get them at other times as well .
We have a daughter who lives close and she is very supportive I an leave him for two or three hours , he prefers not to have a sitter and he can handle the TV I am at the end of the telephone . one press of the button, He doesn't get out of his chair and is PLUMBED in . lol . wears an alarm around his neck . So do I when I am home .
They have also installed a hoist . Unfortunately it is too heavy for me to manage . would make a huge difference it it were easier . We do manage though to transfer from chir to chair without it .
I have a baby monitor at the side of both our beds and a remote doorbell attached to his bed rail .Cant do any more .
We live in Wales so although have to pay for carers it's only £50 weekly however many times they visit . That's at the moment of course .
I will accept any advice or tips and like to share the ones that work for us .
I know not everyone is a able to support their sufferers and it must be dreadful . Sometimes you reap what you sow .
I am going out this evening for two hours , I do look forward to it Althing the first place I found it very hard to go without him .
when sleeping ,natural production of dopamine may be inhibited( his energy tank never gets a chance to get filled because a reserve tank always runs system(sinimet)
the pills may have a negative effect and sustained release pills do not work as well as regular type, in my experience
We have never had the chance to see the Parkinson's nurse . I gave heared that they are the best . Going to try myself to maybe get a home visit .
Diagnosed about 7 years ago at 70 although had been struggling for long time .
It's been difficult to tell how much they have worked becUse we thought it was progression . Not knowing anything about Parkinson's at the time and you ate never given any advice or explanations you are left to your own devices .I don't think they have ever been much help really .
I have told them and always written everything down
They just nod their heads .
I understand that everyone s different and there seems to be different forms of Parkinson's . His half brother same mother has it also he is seven years older and not as bad .
Thank as so much for all your replies . as far as the drugs are concerned you go into in in depth something I am not able to manage to do .
In the first place I think my husband believed it at he aging process , of course like
us all he is aging but until we started to recognised the symptoms he had never ever taken as much as an aspirin if he had an ache or pain he said hE didn't like taking pain killers . The only pain he had was a shouLder pain which had for many years . The same side as his Parkinson's started The droopy shoulder .
I don't think it is mainly
the ageing and its why I keep fighting for him , it's getting them to listen . They have a tick list . He has been taking ths Sinemet and the patch for nearly 7 years but reduced the Sinemet to 110 x3 daily and the 250 CR at night I don't like to play about with too much because I have read that can cause and even bigger problem .
The patch is 6 mg .
He has a rotten few weeks but miracalousy today he is Perkier speaking easier reaching out and responding to movements , I am not expecting it last . He will suddenly switch off his face will change and if I ask him to move he I'll be unable to be stiff as a board anode flop back . Often about an hour aft taking his Sinemet .
I am planning to take some photos of him before and after so that if I cannot get him to the clinic I can show the consultant . With the original consultant we saw him about every 4 months . The last time the caretaker doctor said he will send or us in 6 months .
7 YEARS AND ITS DONE NOTHING, what??WHAT IS POINT IN TAKING DRUGS THAT DONT WORK even worse,TH IS .line dont MESS ABOUT WITH MEDS IS SOMETHING THEY HIDE BEHIND if you don't or cant get something to work, I think hes gonna have to be looked after, FULL TIME NURSE OR CARE HOME but I GUESS YOU KNEW THIS. SORRY CABBAGE PATCHGIRL
In response to the statement that Parkinson's is not one single disease, but many different diseases: as a layman, I have assumed that Parkinson's attacks the substantia nigra, which is not a single brain cell but a whole area of brain cells. It would be foolish to think that the brain cells affected in my brain are the same brain cells affected in anyone else's brain. I would also assume that each brain cell has a function and my affected brain cells affect a certain number of functions, which is bound to be different to everybody else's. But the cause is the same! If this is corrct, then we are on the right track.
Yes, as far as I understand, the faulty cells are in the substantia nigra, a small dark region of the basal ganglia. These cells are responsible for the production of dopamine for use by other areas of the basal ganglia.
One of the functions of the basal ganglia is to decide which way to perform an act. For example, I decide to stand up from the seated position I am in at the moment. This is quite a complex manoeuvre involving many muscle groups. The brain may have several ways to achieve this (pathways) and the basal ganglia selects and initiates one. Furthermore, the basal ganglia can respond to unexpected change and initiate alternate pathways. For example, the arm of the chair collapses under my weight so I grab hold of the desk.
The neurons which do this use the neuro-trasmitter, dopamine, supplied by the substantia nigra. Reduce the supply of the neuro-transmitter and you get the problems in selecting, initiating and changing actions we are all familiar with.
The point I make is none of this is the cause of PD. It is the effects of PD.
GDNF protects and rejuvenates dopamine cells in the substatia nigra. It is an ongoing treatment, not a cure.
Breast cancer (as far as I understand) has multiple causes and a growing number of matching cures. But all have a common symptom - a lump. Could PD be a similar model, the common symptom being the loss of dopamine producing cells in the the substantia nigra?
Hi Grey. Do the glial cells only produce dopamine? Do they have no other purpose? If that is the only purpose of the glail cells, then we are wasting our time looking for ways of repairing or replacing them. I was under the impression that the glial cells were the Parkinson's problem. Fix that problem and you fix Pd. Please put me straight on that one.
Gulp, I'll try, but if a friendly neuro who can speak plain English wishes to but in here then please do.
I understand glial cells to form the environment that ALL neurons require to succeed. This INCLUDES the dopamine producing cells.
There are three types (with fancy Latin names of course):
1 the type that make up the blood brain barrier
2 the type that remove the dead neurons and other garbage
3 there are two sub-types, one acting in the central, the other the peripheral nervous system. Both are to do with the myelin wrapping of the axons. Basically, axons carry the output signal from a cell and can be several feet long. Myelin acts as a protective sheath.
I assume cell damage / death could be failure of the associated glial cells or a direct attack on the cell itself or even self destruct. As far as I understand, the boffins don't have the answer to this yet.
This is the blind leading the blind! So glial cells are not a specific type of brain cell? I thought neurons were another type of brain cell. The ignorance is now showing loud and clear. Maybe some kind person could straighten this all out for us!
john, this science has been explained to you by grey very well
, notta stroll in the park
. glial, glial typecells perform in the main are a background function supportive roll popular glial cell, the macrophheeges the binmen of the system eat debris and aborted cells such that new cells can be grown there are glial cells providing bonding , and isolation etc however
NEURONS(, ( an intelligent cell)that sends a message by a fluid switch operated with dopamine A collection of neurons form a pathway .pathways linking thought to PHYSICAL ACTION,dopaminergenic neurons respond to the transmitter dopamine other neurotransmiters work with mood and feeling their switch operated by another seretonin....dopamine manufactuered from LDOPA, by an enzyme andcofactor derived from food we eat
definition..PARKINSONS dopamine productive cellsIN parscompacta area of substantia nigra . stop producing dopamine and die.the supply of dopamine reduced limits the operation of pathwways some dopamine intensive functions cannot be sustained eg fine hand control is typical
why?/ noDOPAMINE NEEDS 3 THINGS TO HAPPEN 1 is missing
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