Lately I've been wondering why, if amphetamines are a mild MAOI and increase norepinephrine and dopamine, well, why aren't the known MAOIs also used?

It looks like the reason is that people just haven't really made the connection. No doubt the fact that MAOIs are mainly used as secondary treatments for depression, and as treatment for Parkinson's disease doesn't help. Nor the fact that MAO-A inhibitors require strict diet control to avoid risk of death.

So I did a little research on MAO-B inhibitors. These look like the likely target for ADHD meds, because MAO-B doesn't break down serotonin (which I believe is part of the reason MAO-A inhibitors are dangerous). In fact it mainly breaks down phenethylamine and trace amines. And like MAO-A it also breaks down dopamine (both do this equally).

Anyway, in my search it looks like I'm not the only one who has considered this drug's potential. It seems to have the same potency as Ritalin in reducing ADHD symptoms. See favourable analyses here:

The drug Selegiline/Deprenyl

http://www.liebertonline.com/doi/abs/10.1089/cap.2004.14.418?cookieSet=1&journalCode=cap
http://www.selegiline.com/adhd.html
http://www.dr-bob.org/tips/split/MAOIs-for-adult-ADD.html

Best of all, this drug doesn't seem to be regulated, it doesn't seem to cause many (if any) side-effects (in selective doses - i.e. as long as it doesn't inhibit MAO-A), has no abuse potential, and research based on Parkinson's patients indicates that this drug is neuroprotective, and helps fight aging (at least in the brain). Not to mention is seems to have the capacity to positively lift mood, as well.

http://www.selegiline.com/

I do believe I shall try importing some of this to Australia. It seems it gets past customs because it's not scheduled/restricted.

As an interesting side note: the chemical structure is very similar to amphetamine and dopamine. Isn't that always the case eh?

I was reading an article yesterday about Parkinsons, and the symptoms listed (excluding the obvious physical ones) seemed so similar to ADHD..
"loss of memory and concentration"

Yeah Parkinson's is caused by apoptosis of the dopamine producing cells. It makes sense that some symptoms will be familiar. It also worries me that Parkinson's is the end result of ADHD.

Everyone loses a fair amount of dopamine producing cells each decade. When one has lost 70 to 80% of all such cells, you have Parkinson's disease. Do people with ADHD have less of these cells to begin with? Do we have the same number but they produce less? Does this still put us at higher risk of Parkinson's?

I understand why this'd be true - if only in the nuclei associated with Parkinson's (or control of motion) -
is it true that our absolute numbers of dopaminergic cells decreases with time?

argument
-> (may be complete rubbish) <-

---1---
The neurone evolved through the capacity to confer motion
:-)
think worm crawling along and the Faraday effect -
electricity in a coil moving through an EM field.
---2---
Man is aerobically fit - though losing - the capacity to engage in aerobic bursts -
we are not the 'fastest' - though last longer than other more explosive members of the animal kingdom.
---3---
Our evolutionary progress is towards lasting for longer -
though selling our capacity to self propel along the ground -
for something more interesting
---4---
There's a 3 stage pattern in nature
caterpillar -> pupa -> butterfly
---5---
We're in the process of making the pupa/butterfly transition where only
caterpillars need to crawl
---6---
What does butterfly mean in context of man.
->
Imagine a spinning top - which spins every faster and emerges from a pupa as a spinning top -
which cannot be differentiated from a helicopter -

the rotors of the helicopter -
have internal analogue -
electrical flow around the PNS and CNS

and where the lift is obtained by the contrasting EM fields of the person and the planet -

- and where the rhythmic noise of the helicopter rotor -
- is represented by the central oscillator -
the 8 Hz firing rate of the central dopaminergic circuit.

(the steam engine like noise - sinusoidal wave pattern) - made by the helicopter rotor translated into context of mind.
An explanation to
'love gives you wings' -
- and the final stage in our current pattern of evolution.

Yeah Parkinson's is caused by apoptosis of the dopamine producing cells. It makes sense that some symptoms will be familiar. It also worries me that Parkinson's is the end result of ADHD.

Everyone loses a fair amount of dopamine producing cells each decade. When one has lost 70 to 80% of all such cells, you have Parkinson's disease. Do people with ADHD have less of these cells to begin with? Do we have the same number but they produce less? Does this still put us at higher risk of Parkinson's?

dopamine itself is toxic, so taking a small dose of a mao-b inhibitor would be neuroprotective in nature. Also there does seem to be some relationship between parkinsons syndrome and adhd, the diagnostic drug Altropane that is undergoing fda phase II research (Mechanism already established, just testing effectiveness) may be able to diagnose both adhd and parkinsons by means of a brain scan.

Please ignore my previous comment about the dopamine.

'love gives you wings' -

:(trying so hard, to remember what that is.. :)

Dammit, hit back and deleted post.
Anyway, I have been trying to get a doc to prescribe me a dopamine agonist for a long time now to try and help add, major depression/anxiety, bipolar etc.

ah, never heard of thissssb4..

http://www.erowid.org/smarts/selegiline/selegiline.shtml
yes, is available by prescription only

shrugs (i dunno) omg.. oops

ohere is something neatSelegiline retards the metabolism not just of dopamine but also of phenylethylamine (http://chocolate.org/phenylethylamine.htm), a trace amine also found in chocolate (http://chocolate.org/refs/index.html) and released when we're in lovedoubles as anti-aging ...agent..

selegiline's neuroprotective action.:)

Dopamine-related problems in Parkinson's and ADHD are centered around different centers of the brain (from what I can infer). Here's a pretty basic explanation of Parkinson's:

From what I have studied, Parkinson's Disease causes the death of neurons specifically in an area of the mesencephalon (the midbrain) called the substantia nigra pars compacta or SNpc for short. The SNpc sends out neuronal paths to another part of the brain called the dorsal neostriatum. It's here that SNpc neurons release dopamine which either inhibit or promote certain pathways that influence, ultimately, basal ganglial control of movements. The basal ganglia is sort of like a plan of action coordinator. The outer parts of your brain say "hey I want a plan of action" and sends it to the basal ganglia. The basal ganglia sends another message back to the outer part of the brain, saying "hey here's your plan." If you don't have a working SNpc, you will have an overactive part of the basal ganglia called the subthalamic nucleus. This inhibits signals for movement--and so if it is overactive, you have slow, difficult conscious movements. If you've ever heard of Huntington's disease, it pretty much does the opposite, although the mechanism of action is slightly different.

ADHD, on the other hand, is related more to the limbic system, our reward pathway. I haven't studied that yet too extensively, but from what I have read, the drugs for Parkinson's are aimed to specifically take the place of the SNpc's action. Drugs for ADHD generally work by taking the place of dopamine in dopamine releasing parts of the limbic system and therefore cause a mass release of dopamine (this last part I have read through various websites, but I can't confirm with my own studies--just a first year med student, not quite done with everything in the books yet)

So ultimately, taking drugs like L-dopa might screw up your basal ganglial regulation of movement (I'm assuming--haven't taken pharmacology yet), and I'm not sure if they would benefit ADHD.

Hope that wasn't too much info :-D Helps me memorize stuff--got a neuro test tomorrow.

Parkinsons is the end result of ADHD?? Are you serious? I've just had a friend's Dad diagnosed with Parkisons - i don't want it.:(

Parkinsons is the end result of ADHD?? Are you serious? I've just had a friend's Dad diagnosed with Parkisons - i don't want it.:(

No, no! I was just suggesting that it might be related. Maybe the genetic cause of Parkinson's is the same as that of ADHD, or related to the genetics of ADHD? But equally likely, maybe not.

So I did a little research on MAO-B inhibitors. These look like the likely target for ADHD meds, because MAO-B doesn't break down serotonin (which I believe is part of the reason MAO-A inhibitors are dangerous). In fact it mainly breaks down phenethylamine and trace amines. And like MAO-A it also breaks down dopamine (both do this equally).




............http://upload.wikimedia.org/wikipedia/commons/thumb/f/fe/Fenyloetyloamina.svg/200px-Fenyloetyloamina.svg.png


it's a pretty structure

......roundabout --- highway --- aNcH2or

..pi electrons - 1 / 2 \ 3 ---N(7) less stable than C (6)

----------------<-------------<---------- earth,ground.
-/. - - - - - - - - - - - - - - - e- - - -- - - - - - - - - - - - - - - --N pushes 'em away
v
-\
---------------------------------->--------------------------
v - - - - - - - - - - - - - - - e- - - - - - - - - - - - - - - - - - - - - and then N welcomes 'em back

.................................................. .................................................. ............................................_ _ _ _
.................................................. .................................................. .......................................|.......... ..............|

- - - - - - - - - - - - - -|sn| <- repel...................|.North .| pole
.
.
- - - - - - - - - - - - - -|sn| attract ->...........|South..| pole
..
.................................................. .................................................. ......................................|_ _ _ _|

of a bar magnet



then recharacterize the bar magnet and the electron as follows

S >|< N

-> all emergent structures fast switch between bipolar states in everted 3d spaces

So - moving as follows
>
>|
>|<
>|
>

-> net effect ->
N__
____\
_____S
-> not 2d symmetry in 3d - but 3d eversions (see below - a bit bent'd be a 'loose' description of shapes of two everted halves)

- we can see how NH2 would act as a repellent :-) to a smaller S >|< N
structure in one orthogonal space - and in the adjacent orthogonal space -
it'd act as an attractor

- so if we see the electron as travelling from one orthogonal 3d space to another -
we observe an electrical circuit here -
where the repellent action of
N pole of NH2
on
N pole of electron

until the soma (head) is reached -
whereupon the smaller structure switches and so the electron turns the corner -
and instead of the
repulsion of
N pole of NH2
on
N pole of electron

the
S pole of NH2
attracts
the N pole of electron

a circuit is formed by the transition from one orthogonal space into another via an eversion -

the important feature of this process -
is that the two eversions in different spaces -
can appear to be in the same space -

however they are not -

- are subtly off -

and Picasso's representation of the face of woman being non-symmetrical is a clear sign that the evolutionary event which marks out

ADDers (Homo neosapiens) (post-modern man)
versus
modern man (Homo sapiens)

- that ADDers (we) have greater capacity to model reality -
within our own minds

- so -
formerly we'd have regarded a woman's face as a kinda' two symmetrical halves in 2d -
->- interpolated into 3d

however that is not correct -
- the 'Picasso' below is an attempt to make the correction to balance the eyes of mind of ADDer with the eyes of nonADDer
- to usurp the mind of nonADDer

modern man (animal) (nonADDer) (first stalked the Earth around 30k years ago)

->- speciation event ->-

ADDer ***now***


Through eyes -> mind of nonADDer

http://tbn0.google.com/images?q=tbn:YlVNzxSVMC0KIM:http://img266.imageshack.us/img266/8035/picture19cm4.jpg

Through eyes -> mind of ADDer

http://tbn0.google.com/images?q=tbn:NtS8rqVLiUmneM:http://www.instituto-picasso.com/learn-spanish/picasso3.jpg

............http://upload.wikimedia.org/wikipedia/commons/thumb/f/fe/Fenyloetyloamina.svg/200px-Fenyloetyloamina.svg.png
...............head..-......body...-....tail

---1---
smells fishy


---2---
looks fishy

http://tbn0.google.com/images?q=tbn:IkVWDYD0x2Iy3M:http://pinkzap.com/wp-content/uploads/2007/07/fish.jpg

head -body -tail

---3---
is called PEE


(nearly)
:-)

http://en.wikipedia.org/wiki/Phenethylamine
Phenethylamine

at least in my world
http://en.wikipedia.org/wiki/Phenethylamine
Phenethylamine

well, why aren't the known MAOIs also used?Sometimes they are used, but just not as regularly. There are many more side effects/diet restrictions that one needs to be very cautious about with the MAOIs, especially the older generation ones. From the Mayo Clinic website:

http://www.mayoclinic.com/health/maois/MH00072

MAOIs can cause dangerous interactions with certain foods and beverages. If you take MAOIs, you'll face dietary restrictions that require you to limit consumption of foods that contain a high level of tyramine, such as many cheeses, pickled foods, chocolates, certain meats, beer, wine, and alcohol-free or reduced-alcohol beer and wine. The interaction of tyramine with MAOIs can cause a dangerously high increase in blood pressure, which can lead to a stroke. Your health care professional can give you a complete list of dietary restrictions. The stimulants work "better" and have a lower side effect profile, so that's why they're used more often than the MAOIs.

It may be that MAOB inhibitors have a less severe side effect profile, but I don't know that for sure.

The Parkinson's drugs (L-DOPA) work in part becuase there are less neurons producing dopamine, and therefore the amount of precursor product makes a difference (the remaining neurons are working full out and unable to cope with deficiency). If you've got differences at the level of the receptor/transporter (like in ADHD), I don't think the drugs work as well, partially because there is such a strong pull towards balancing out the amount of dopamine the neuron is making. In other words, in ADHD the amount of dopamine being made by the neurons is "normal", it is the way the dopamine interacts with other neurons that's the problem. The stimulants are more effective because the act directly at the level of the transporter.