Editor's note:

The article reflects the opinion of our author, describes his use of the drug and justifies this to the best of our knowledge and belief. In no case does it replace the advice of your doctor and should under no circumstances lead to self-medication.

Wikipedia describes rasagiline as follows:

Rasagiline is a potent, irreversible and selective inhibitor of monoamine oxidase B (MAO-B). The active ingredient leads to an increase in extracellular dopamine levels in the striatum. The resulting increased dopaminergic activity likely mediates the beneficial effects of rasagiline in Parkinson's disease.

Rasagiline - Why everyone should take it.

There was a discussion here recently in a Facebook group. "Well I've been on rasagiline for 2 weeks
and it didn't help, so I left it out again." "It was the same for me."
"I had the following side effects on it:" etc.

All of this didn't convince me. Because I've been taking rasagiline since the beginning and I definitely will
Keep case to the very last. And I think everyone should have it at their
have a mix of medicines with you. A drug combination without rasagiline seems to me
illogical.

Before you simply refuse a drug, you should know what to expect from it and
what not. And if you want to understand your illness and medication treatment,
you should also know how rasagiline works.

PS: When I talk about rasagiline (trade names include: Azilect®, Rasagea®), I also mean others
Drugs such as selegiline or safinamide (Xadago®). One of the three is sufficient. So,
one of these three drugs should be included in any combination therapy.

How does rasagiline (or selegeline or safinamide) work?

We should repeat how the Parkinson's symptoms develop.

The Parkinson's specific process of nerve damage has been going on for a while. But now
it has reached the substantia nigra: a small, inconspicuous structure in the lower brain stem, whose
You only learn to appreciate meaning when it is no longer fully there. In the nerve cells
namely, dopamine is formed in the substantia nigra. This dopamine is produced via the long (2 cm)
Extensions of this cell, the nerve fiber, are conducted into the striatum. There it gets into the synaptic
poured out and thus stimulates the following nerve cell in the striatum. In this synaptic
However, there is an enzyme lurking in the gap, the MAO-B = the type B monoamine oxidase, which extends the lifespan
and thus shortens the duration of action of dopamine.

We only get our first Parkinson's symptoms when more than half of them are gone
substantia nigra cells have died and one consequently appears in the few remaining synapses
every bit of dopamine is badly needed. And since this monoamine oxidase B can only interfere.
If only we could stop them...

And that's exactly what we can do. Rasagiline, selegiline and safinamide block this enzyme. carry with it
they help us get more impact from the remaining dopamine.

Rasagiline acts indirectly

Anyone who has paid close attention will notice that rasagiline alone does not work at all. It only works via the detour of
dopamine. Namely via the residual dopamine, which we use at the very beginning of our illness
feature. And later about the dopamine that we swallow as a drug.

So without dopamine, rasagiline doesn't work at all. It's from all the medicines we take
probably the weakest.

Why should we start rasagiline?
At the very beginning of our illness we still have quite a lot of dopamine and only one whole
minor deficiency. It could be that rasagiline is sufficient as the only drug for a short time.
So we start with rasagiline solo.

2 options:

• We are really still at the beginning. Rasagiline works. The small increase in our
Dopamine action is enough, and we're better.
This is possible, but quite unlikely:

• Rasagiline alone is not sufficient. Then we should continue to take rasagiline (and not
drop!!!) and combine it with a dopamine agonist or dopamine. At least now
we are better What part rasagiline has played in our recovery we'll never know
experience.

Rasagiline in advanced disease stages

In advanced stages we need - and sometimes not a little - Levo-Dopa so that it
converted to dopamine in the brain. And suddenly the rasagiline gets a new meaning:
It helps the dopamine, which comes from the drugs, to have a better and more balanced effect.
Anyone with advanced Parkinson's disease (and not on deep brain stimulation) can see how
dependent on Levo-Dopa. If we don't have enough, we can hardly move, the muscles
become stiff and the tremors worsen. If we have too much, we start to strengthen ourselves and
sometimes too tense to move, can no longer sit still, etc. And the longer we die
If you have a disease, this back and forth between overdose and deficiency is all the more annoying.
The phases in between, where the drug effect is right, are becoming shorter and shorter.

If the disease progresses and the brain that from the drugs
originating dopamine can no longer be cached, we notice the big problem that
Levodopa has: The duration of action is too short at 2-3 hours. Oh, if only there were something that
Duration of effect extended!

And here we have two candidates:

1. The MAO-B inhibitors, i.e. rasagiline, selegiline or safinamide.

2. The so-called COMT inhibitors (tolcapone = Tasmar®, entacapone = Comtess®, fixe
Combination of Levo-Dopa + Carbidopa + Entacapone = Stalevo®, Opicapone = Ongentys®).
COMT (catechol methyl transferase) also nibbles away dopamine.

With one of these drugs we can block this enzyme and the duration of action of Levo-Dopa
extend, so can above all avoid "end-of-dose" problems.
And there is absolutely no reason not to combine MAO-B inhibitors and COMT inhibitors.

So this is what a logically and sensibly packaged looks like
combination of drugs in an advanced stage
• Rasagiline (or selegiline or safinamide)
o A dopamine agonist
▪ Levo-Dopa
• A COMT inhibitor, preferably opicapone = Ongentys

There is another reason to stay on rasagiline all the time.

It is clear to all of us that the drugs only affect the symptoms, not the process
of nerve cell death and thus the progression of the disease. With a
Exception:
In the case of rasagiline in particular, there was once hope that this drug could also stimulate nerve cells
can protect. Not many people believe that, but as we all know, hope dies last.
I wouldn't want to stop rasagiline if I had to???

And to finish
I'm a doctor, but not a neurologist. So just take this file as food for thought. Or take them to your neurologist and
ask him why you're not getting rasagiline.

Greetings from the off (fortunately not from the dopamine off)
Your Johannes