How about developing a new machine on the lines of a kidney dialysis machine, so that a PD sufferer can be connected up, have an automated blood test for all the key blood components and elements, then based on the results and some pre-set parameters for the particular patient, the blood then gets filtered and dosed with the ideal mix / concentration of Dopamine, minerals, proteins, enzymes etc. This may produce far better results than all the usual meds which often end up in the wrong concentrations. We need to deal with the blood directly. I know that the drug companies will oppose this, even though it makes good sense ....... that's because they making pots of money out of sales of all these drugs which make our lives miserable and ruin our health. Let's see a really significant scientific & medical breakthrough on this, the technology exists, it can be done ! We just need someone with a a bit of vision to pick up the batton and run with it !
What a darn good idea. It makes sense, wonder why the powers that be have never thought about this?
Might the reason be that dopamine (insufficient formation & lack of acivity of of, which is established as the neurogenic cause of pd symptoms, if not the actual root cause of the disease) does not cross the blood / brain barrier ? Thus whilst blood tests can identify lack or indeed excess of certain key elements, they can tell us nothing about the level of dopamine , let alone what might be a therapeutic dose?
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L-DOPA, LEVODOPA and DOPAMINE
L-DOPA is made and used as a part of the normal biology of humans and some other animals and plants. It is made via biosynthesis from the amino acid L-tyrosine. L-DOPA is the precursor to certain neurotransmitters, including Dopamine, collectively known as catecholamines. L-DOPA can be manufactured, and in its pure form this artificial drug is known as Levodopa. Trade names include Sinemet, Madopar, Stalevo, etc). As a drug it is used in the clinical treatment of Parkinson's and Dopamine-responsive dystonia.
L-DOPA crosses the protective blood-brain barrier (BBB), whereas Dopamine itself cannot. Thus, L-DOPA is used to increase Dopamine concentrations in the treatment of Parkinson's disease and Dopamine-responsive dystonia. Once L-DOPA has entered the central nervous system, it is converted into Dopamine by the enzyme DOPA decarboxylase (DDC). Pyridoxal phosphate (vitamin B6) is a required cofactor in this reaction, and is sometimes administered along with L-DOPA, usually in the form of Pyridoxine.
Besides the central nervous system, L-DOPA is also converted into Dopamine from within the peripheral nervous system. The resulting hyperdopaminergia causes many of the adverse side effects seen with sole L-DOPA administration. To bypass these effects it is standard practice to co-administer (with L-DOPA) a peripheral DOPA decarboxylase inhibitor (DDCI) such as Carbidopa (e.g. in Sinemet) or Benserazide (e.g. in Madopar), to prevent the peripheral synthesis of Dopamine from L-DOPA. Co-administration of Pyridoxine without a DDCI accelerates the peripheral decarboxylation of L-DOPA to such an extent as to negate the effects of L-DOPA administration. Historically this phenomenon caused much confusion.
In addition, L-DOPA, co-administered with a peripheral DDCI, has been investigated as a potential treatment for restless leg syndrome. However, studies to date have demonstrated "no clear picture of reduced symptoms".
The two types of response seen with administration of L-DOPA are:
(a) Short-duration response, which is related to the half-life of the drug;
(b) Longer-duration response, which depends on the accumulation of effects over at least two weeks. This response is evident only in early therapy, as the inability of the brain to store Dopamine is not yet a concern.
.
L-DOPA, LEVODOPA and DOPAMINE
L-DOPA is made and used as a part of the normal biology of humans and some other animals and plants. It is made via biosynthesis from the amino acid L-tyrosine. L-DOPA is the precursor to certain neurotransmitters, including Dopamine, collectively known as catecholamines. L-DOPA can be manufactured, and in its pure form this artificial drug is known as Levodopa. Trade names include Sinemet, Madopar, Stalevo, etc). As a drug it is used in the clinical treatment of Parkinson's and Dopamine-responsive dystonia.
L-DOPA crosses the protective blood-brain barrier (BBB), whereas Dopamine itself cannot. Thus, L-DOPA is used to increase Dopamine concentrations in the treatment of Parkinson's disease and Dopamine-responsive dystonia. Once L-DOPA has entered the central nervous system, it is converted into Dopamine by the enzyme DOPA decarboxylase (DDC). Pyridoxal phosphate (vitamin B6) is a required cofactor in this reaction, and is sometimes administered along with L-DOPA, usually in the form of Pyridoxine.
Besides the central nervous system, L-DOPA is also converted into Dopamine from within the peripheral nervous system. The resulting hyperdopaminergia causes many of the adverse side effects seen with sole L-DOPA administration. To bypass these effects it is standard practice to co-administer (with L-DOPA) a peripheral DOPA decarboxylase inhibitor (DDCI) such as Carbidopa (e.g. in Sinemet) or Benserazide (e.g. in Madopar), to prevent the peripheral synthesis of Dopamine from L-DOPA. Co-administration of Pyridoxine without a DDCI accelerates the peripheral decarboxylation of L-DOPA to such an extent as to negate the effects of L-DOPA administration. Historically this phenomenon caused much confusion.
In addition, L-DOPA, co-administered with a peripheral DDCI, has been investigated as a potential treatment for restless leg syndrome. However, studies to date have demonstrated "no clear picture of reduced symptoms".
The two types of response seen with administration of L-DOPA are:
(a) Short-duration response, which is related to the half-life of the drug;
(b) Longer-duration response, which depends on the accumulation of effects over at least two weeks. This response is evident only in early therapy, as the inability of the brain to store Dopamine is not yet a concern.
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that's a remarkably concise and comprehensive description, never seen one as good.
M and I are going to a parkinson's education course at the local hospital. the rather lovely doctor said two things. One about the difficulty of Ldopa getting through the stomach and the other about the quickest way to the brain being through the nose.
I really wanted to ask him if it would be a good idea to sniff it but didn't quite have the courage. One because I suspect he was already finding me a bit much with my questions and two because he might think I was a cocaine user (I'm not!) Still wondering though.
I really wanted to ask him if it would be a good idea to sniff it but didn't quite have the courage. One because I suspect he was already finding me a bit much with my questions and two because he might think I was a cocaine user (I'm not!) Still wondering though.
The second most inefficient way of getting a drug into the brain is via the stomach (or the intestines, I dont know all the details but different bits of the gut absorb differently). A large part of drugs go straight out or are affected by food or used in the periphery.
The next best is into the bloodstream.
then there is the lungs.
but the best is the nose - there is a direct service from the nose to the brain. it is after all stuck right in front of it and our distant ancestors probably relied on it more than any other sense (think mice or voles).
there are even theories and evidence that PD is essentially a nasal disease that secondarily affects the brain. loss of sense of smell is supposedly one of the tell-tale signs.
if the nose is the source of pd it would be fittingly ironic if a cure could be administered along the same route.
The next best is into the bloodstream.
then there is the lungs.
but the best is the nose - there is a direct service from the nose to the brain. it is after all stuck right in front of it and our distant ancestors probably relied on it more than any other sense (think mice or voles).
there are even theories and evidence that PD is essentially a nasal disease that secondarily affects the brain. loss of sense of smell is supposedly one of the tell-tale signs.
if the nose is the source of pd it would be fittingly ironic if a cure could be administered along the same route.
Hi Turnip
What you say makes sense why the Duadopa infusion that administers the drug directly into the Duodenum has this gives optimum benefit.
If the tube moves into the stomach and not working properly you would get symptoms.
Therefore the administration via this route if available to more people in the UK if accepted by NICE would surely be a benefit ?
Regards
What you say makes sense why the Duadopa infusion that administers the drug directly into the Duodenum has this gives optimum benefit.
If the tube moves into the stomach and not working properly you would get symptoms.
Therefore the administration via this route if available to more people in the UK if accepted by NICE would surely be a benefit ?
Regards
http://intranasal.net/AnatomyPhysiology/default.htm#Nose-brain_pathway_
'intranasal.net' - what a great name for a web site. the nose brain pathway 'skips the blood brain barrier'. Its not really that much of a barrier if you can get round it by sticking something up your nose.
'intranasal.net' - what a great name for a web site. the nose brain pathway 'skips the blood brain barrier'. Its not really that much of a barrier if you can get round it by sticking something up your nose.
hi Bubble X
I didnt realise it wasnt accepted by NICE. They seem to take a long time to review procedures. Drug delivery options must be one of the research areas that could make a big difference fairly quickly. Particularly to those who have problems with nausea. The nasal route looks very interesting-but what happens if you have a cold???
I didnt realise it wasnt accepted by NICE. They seem to take a long time to review procedures. Drug delivery options must be one of the research areas that could make a big difference fairly quickly. Particularly to those who have problems with nausea. The nasal route looks very interesting-but what happens if you have a cold???
My thoughts turn to the possible effects upon the nasal septum of "sniffing" pd drugs
absoooolutely AB. sniff sniff. Every mode of input has its problems. on the upside it would allow the input of pure dopamine rather the l-dopa (so no chemicals needed to stop peripheral conversion), it would be i think about 50x more effective (ie 1/50th of the volume) and possibly not as often. Perhaps it would be used in conjunction with the oral route. I'm not one for knocking the big pharms over research but this might be a real case where there is no incentive for investment.
hey all at the forum has anyone heard of prosavin its a new treatment being researched at oxford medica they have started phase 1 of research by injecting prosavin into the brain i have heard results are promising
I have heared the same about that drug ... Looks promising ..
We had a request for a donation for one study , can't remember which one . It said they hoped it would be for a cure in the researchers lifetime .. Then I noticed he only looked about 30 ..
We had a request for a donation for one study , can't remember which one . It said they hoped it would be for a cure in the researchers lifetime .. Then I noticed he only looked about 30 ..