View Full Version : Aricept (Donepezil) for ADD memory issues?
07-12-05, 06:59 PM
Does anyone out there have experience (first, second, thirdhand...) with using donepezil or similar Alz meds to treat ADD? I keep coming across references in the literature.
60mg of Dex per day does wonders for energy and concentration, but if only my memory and "executive functioning" was helped as much...
07-14-05, 07:39 PM
it's my strong opinion that the old robots from I-Robot will be for real
in the near future like that FedEx robot which btw I want one of those to do my cooking, cleaning, what not. Probablly will cost me 5,000 dollars for my robot anyways. My point is within a few years there will be medication for minimal brain damage, surgery to fix shrinkage of brain tissue if a person was to have that problem. As well there will be something that will discontinue the use of Ritalin, Adderall ~no pun intended~
seriously to anyone that of which is helping them for now cause imo
I would think all of you would prefer a really good non stimulant for AD/HD.
By the year 2006-2008 you'll see a break through in medical science like
never seen before a miracle to all whom need medicine that want a medicine
that works especially for long term use that has no negative effects of usage.
And surgery, or medication to help with any minimal brain damage
so you'd be all good again.
07-15-05, 10:01 AM
Please stop wasting my time MillenniumMan.
For information on medications and supplements that can help memory, please consult http://www.imminst.org/forum, in particular search posts made by LifeMirage. You will be interested in the "Nootropics & Brain Enhancers" forum.
07-15-05, 05:52 PM
I don't waste anyone's time sir Chadwick.
I look out for people and for one your not in my shoes
now are you but thanks for the hyperlink.
07-15-05, 07:30 PM
Please do try to stay on topic MillenniumMan. There are areas of the forum for all kinds of discussions but this particular thread is a request for information on a particular drug - and sorry wilbur, but I don't know anything about that particular drug. I'll see what I can find out.
I'm trying to find out everything I can about this drug which I only heard of a day ago. Wilburr, my guess is that you have had to live with the personal assaults on your character due to your memory/attention impairments for your entire life, due to the ignorance of judgemental people with no desire to learn empathy. I certainly have. I do know, that if my disability were "visible", for example, Tourettes, no one would say the cruel things said to me over the years. My point? LOL, that being scrutinized for taking a particular medication is, by comparison, a fly buzzing by your ear. ( ;
09-10-05, 12:46 AM
I haven't heard anythig yet about Aricept specifically, Wilburr, but thanks for the heads up. I'll check it out straight away. There are a number of non-stimulant med that have benefitted ADD/ADHD, however. Possibly the most established is Selegiline, (Deprenyl) which was used originally for treatment of Parkinson's Disease and then later, for Alzheimer's. As you might know, Parkinson's etiology is Dopamine related, as well, although completely differrent in expression, of course. Selegiline is a b-Mono Amine Oxidase Inhibitor, as opposed to the old MAOIs used as antidepressents. Anyway, turns out there's more than one kind of MAOI, and unlike the old, a-MAOIs--which you couldn't eat anything containing trytophan while you were taking, or it would actually KILL you. That means no cheese, red wine, turkey, etc. etc. (it's called a "cheese reaction"...great name). B-Monoamine oxidase breaks down Dopamine...so, "inhibit" it with Selegiline, and presto, more dopamine available in the synaptic cleft. Even better, there's apparantly reliable data that it provides significant protection to not only neurons, but myelin sheaths (I don't remember exactly where I read this, now, but it was mentioned in a few respected journals, as I remember. I think I copied it, and will look if anyone would like to know the source, though you should be able to pull it up with a google search). In addition to that, it acts as an antioxidant...and finally, it's been demonstrated to extend the lives of rats! So if you have some old rats around you've grown attached to, now you know what to do!..but seriously...it's listed by a number of entirely non-commercial, research-oriented resources as being "likely to possess life-extending properties", do with that what you will. It potentiates the effects of ritalin and amphetamines, of course, and it's cheaper by a longshot, so it would seem as though it could be employed for its economic advantages, at the least. O.K, I just ran a search on Yahoo search on "Deprenyl and phenylethylamine"---as I knew that trials had been done with Deprenyl and phenylethylamine demonstrating that both had better success in alleviating depression and anxiety than did the gamut of available antidepressants---and I found this info....under the first entry, listed as "Home"---apparantly an article in "International Antiaging Magazine", entitled "Extending Optimal Healthspan with Deprenyl by James South, MA" :
[Ed.- Deprenyl is one of the mainstays and still one of the most important drugs used in Antiaging Medicine today. It has been shown to have a wide diversity of uses, including slowing and treating the prevalence of dementia (in particular Parkinson’s and Alzheimer’s Disease), and is also a potent anti-depressive, as well as a libido enhancing agent. Furthermore, it has significantly increased the life span of animals. How can one substance have such a wide diversity of effects? This article attempts to highlight the actions and issues surrounding deprenyl and detail some of its uses].
Deprenyl is a drug that was discovered around 1964 by Dr. Joseph Knoll and colleagues, and was originally developed as a “psychic energizer.” Also known as L-deprenyl and selegiline, it has been intensively researched over the past 40 years with many hundreds of research papers having been published. When reviewing them, it becomes apparent that deprenyl has a unique and exciting profile. It is the only potent, selective MAO-B inhibitor in medical use, plus it is a “catecholamine activity enhancer.”
In addition, deprenyl has been shown to protect nerve cells against a wide range of neurotoxins, and to act as a “neuroprotection agent” when nerve cells are exposed to damaging or stressful conditions.
Today, deprenyl is a recognised treatment for Parkinson’s disease, but it is also useful in treating depression. Furthermore, in aged animals, deprenyl has proven to be a highly effective “sexual rejuvenator” and also shows promise as a cognitive enhancement agent.
Deprenyl has been proven, in four different rodent studies, and one dog study, to be a remarkable life-extension agent.
It was in 1971 when Dr. Knoll showed that deprenyl was a unique kind of MAO inhibitor– specifically a selective MAO-B inhibitor, without any “cheese effect.” Effectively by inhibiting this enzyme, deprenyl can increase the brain’s levels of dopamine, and while some authors have questioned deprenyl’s ability to increase dopamine levels by this method alone, it wasn’t until the 1990s that Dr. Knoll discovered the “main basis” of deprenyl’s action.
Jozeph Knoll, M.D., PharmD., is the Professor of Pharmacology at the University of Semmelweiss, in Hungary. His long career has seen him achieve numerous innovative medical and pharmaceutical breakthroughs, including the development of tests for pharmacological analysis of tranquillizers and psychostimulants. Plus his analysis of the physiological basis of drive-motivated behavior created new analgesic anti-inflammatory drug groups. In the 1960s he was a key-player in the development of deprenyl. His experiments have shown it to slow the age-related decline of sexual and learning performance and prolong life. He is also a recipient of the Monte Carlo Award for Excellence in Anti-Aging Medicine.
Attention, Depression, Life Span and the Catecholamines
During the 1990s Dr. Knoll uncovered a new mode of action of deprenyl that he believes explains its widespread clinical utility. He discovered that deprenyl (and its “cousin”- phenylethylamine) are “catecholamine activity enhancers.”
Catecholamines refer to the inter-related neurotransmitters of dopamine, noradrenaline and adrenaline. These transmitters activate key brain circuits helping to maintain focus, concentration, alertness and attention. Dopamine is also the transmitter for a brainstem circuit that connects the substantia nigra and the striatum, helping control bodily movement and which partially dies off and malfunctions with Parkinson’s disease.
When an electrical impulse travels down the length of a neuron, from the receiving dendrite, through the cell body, and down the transmitting axon, it triggers the release of packets of neurotransmitters into the synaptic gap. These transmitters hook onto receptors of the next neuron, triggering an electrical impulse which then travels down that neuron, causing yet another transmitter release. What Dr. Knoll and colleagues discovered through their highly technical experiments, is that deprenyl and phenylethylamine act more efficiently to couple the release of neurotransmitters.
Deprenyl causes a larger release of transmitters in response to a given electrical impulse. It’s like “turning up the volume” on catecholamine nerve cell activity. This may be clinically very useful in various contexts such as Parkinson’s and Alzheimer’s disease, where the nigrostriatal tract and neural circuits under-function. It can also be useful in depression, where there may be under-activity of both dopamine and noradrenalin neurons.
Dr. Knoll’s research indicates that after sexual maturity, the activity of the catecholamine nervous system gradually declines, and that the rate of this decline determines the rate at which a person or animal ages.
Therefore, Dr. Knoll believes that deprenyl’s positive catecholamine effect explains its antiaging benefit. In addition, his work indicates that phenylethylamine is also a catecholamine substance. Phenylethylamine is a trace amine made in the brain that modulates (enhances) the activity of dopamine and noradrenaline neurons. Autopsy studies have shown that while deprenyl increases dopamine levels in a Parkinson’s patient brain by 40% to 70%, deprenyl increases phenylethylamine levels by 1300% to 3500%. Phenylethylamine is the preferred substrate for MAO-B, the MAO that deprenyl inhibits. Paterson and colleagues have shown that phenylethylamine has an extremely rapid turnover due to its rapid and continuous breakdown by MAO-B. Thus deprenyl’s catecholamine activity has a dual mode of action. At low, non MAO-B inhibiting doses, deprenyl has direct catecholamine enhancing activity.
At higher, MAO-B inhibiting doses, deprenyl creates an additional catecholamine effect, due to the huge increases in brain phenylethylamine levels that deprenyl causes, (phenylethylamine also being a catecholamine substance). Many authors have pointed out the probable dopamine neuron activity enhancing effect of phenylethylamine in Parkinson’s patients taking deprenyl. Therefore, Dr. Knoll’s discovery of phenylethylamine’s catecholamine effect now explains this phenylethylamine/ dopamine-enhancing effect.
Deprenyl has been shown to protect nerve cells from an ever-growing list of neurotoxins. Some of these neurotoxins can actually be produced within the brain under certain conditions, while others come from the environment or diet. Some of these neurotoxins are noted below:
• MPTP is a contaminant in synthetic heroin, however compounds with a chemical structure similar to MPTP, include both natural and synthetic products, (e.g. paraquat), and are used in agriculture!
• 6-OHDA, is a potent neurotoxin that can spontaneously form from dopamine in dopamine using neurons. 6-OHDA may then further auto-oxidize to generate toxic superoxide and hydroxyl free radicals and hydrogen peroxide. Dr. Knoll’s research has shown that pre-treatment of striatal dopamine-neurons with deprenyl can completely protect them from 6-OHDA toxicity. Even in those not suffering from Parkinson’s disease, the nigrostriatal neurons are the fastest aging neuron population in the human brain- with an average 13% loss every decade from the 40s on. Dr. Knoll and others believe that 6-OHDA neurotoxicity is a key cause of this “normal” nigral death, and that deprenyl may be able to retard this debilitating downhill neural slide.
• DSP-4 is a synthetic noradrenaline nerve toxin. In rodents, deprenyl has been shown to prevent the depletion of noradrenaline that DSP-4 causes.
• AF64A is a cholinergic toxin- it damages brain cells that use acetylcholine, (the neurotransmitter primarily affected in Alzheimer’s disease). Deprenyl has been shown to protect cholinergic neurons from AF64A toxicity.
• Deprenyl has also protected human nerve cells from peroxynitrite and nitric oxide toxicity.
• Methyl-salsolinol is another MAO-B produced endogenous neurotoxin. Salsolinol is produced from the interaction of dopamine and acetaldehyde, (the first-stage breakdown product of alcohol). By inhibiting MAO-B, deprenyl reduces the toxic load on the brain that is routinely produced through the normal operation of MAO-B. MAO-B digests not just dopamine and phenylethylamine, but also tryptamine, tyramine and various other secondary and tertiary amines.
• The above are just some of the many reports in the scientific literature on deprenyl’s versatile neuroprotection.
(article goes on to discuss deprenyl in parkinson's disease...)
Alzheimer’s disease is the most widespread neurodenerative disease of modern times, affecting several million people in the U.S. alone. Alzheimer’s is characterized not only by severe memory loss, but also by verbal dysfunction, learning disability and behavioral difficulties, even hallucinations. Alzheimer’s is known to involve damage to the cholinergic neurons of the hippocampus, but in addition to the reduction of acetylcholine, alterations have been observed in the activities of other neurotransmitters. In particular, cerebral depletion of dopamine can lead to memory and attention deficits, plus in Alzheimer’s there is significant increase in MAO-B.
Thus, with its combined MAO-B inhibition effects and catecholamine activity enhancing effects, deprenyl would seem “tailor-made” to treat Alzheimer’s. Indeed, that is the conclusion of a 1996 review paper on Alzheimer’s and deprenyl.
Tolbert and Fuller reviewed 4 single-blind and 2 open label deprenyl trials in Alzheimer’s, as well as 11 double-blind deprenyl/Alzheimer’s studies. They noted that all 6 of the single-blind/open label studies reported positive results, while 8 of the 11 double-blind studies reported favorable results, typically utilizing a 10 mg deprenyl/ day dosage. In 3 of the single-blind studies deprenyl was compared to 3 Nootropics, oxiracetam, phosphatidylserine and acetyl-L-carnitine, and deprenyl was superior to all 3. Tolbert and Fuller were so impressed with deprenyl that they concluded; “...in our opinion, [deprenyl] is useful as initial therapy in patients with mild-to-moderate Alzheimer disease to manage cognitive behavioral symptoms. In patients with moderate-to-severe Alzheimer disease, [deprenyl’s] efficacy has not been adequately assessed. However, given the lack of standard treatment, selegiline should be considered among the various treatment options.”
Deprenyl has been used experimentally as a treatment for depression since the late 1970s. While the causes of depression are diverse, it is by now accepted that dysfunction of dopamine and noradrenaline neural systems is a frequent biochemical cause of depression.
In addition, the research of A. Sabelli and colleagues has established that a brain phenylethylamine deficiency also seems to be strongly implicated in many cases of depression. Given that deprenyl is a catecholamine activity enhancer, and that deprenyl strongly increases brain phenylethylamine through MAO-B inhibition, deprenyl would seem a rational treatment for depression.
Studies with atypical depressives, treatment-resistant depressives and major depressives have shown deprenyl to be an effective, low side-effect depression treatment. However, such studies have often required deprenyl dosages in the 20 mg or even 30 mg range. While these dosages caused little problem in these short-term studies, it is dubious to consider using such very high, non-selective MAO-B inhibition doses for long term treatment, (e.g. months or years).
In 1978, Mendelwicz and Youdim treated 14 depressed patients with 5 mg deprenyl plus 300 mg 5-HTP three times daily for 32 days. Deprenyl potentiated the antidepressant effect of 5-HTP in 10 of the 14 patients. 5-HTP enhances brain serotonin metabolism, which is frequently a problem in depression, while deprenyl enhances the dopamine/ noradrenaline activity. Under-activity of brain dopamine, noradrenaline and serotonin neural systems are the most frequently cited biochemical causes of depression, so deprenyl plus 5-HTP would seem a natural antidepressant combination.
In 1984, Birkmayer, Knoll and colleagues published their successful results in 155 unipolar depressed patients who were extremely treatment-resistant. Approximately 70% of their patients given 5 mg to 10 mg of deprenyl plus 250 mg of phenylalanine daily, achieved full remission, typically within 1-3 weeks. Some patients were continued for up to 2 years on treatment without loss of antidepressant action. The combination of deprenyl plus phenylalanine enhances brain phenylethylamine activity, while both deprenyl and phenylethylamine enhance brain catecholamine activity. Thus, deprenyl plus phenylalanine is also a natural antidepressant combination...."
I'm tempted to include the entire article, I believe getting the word out about Selegeline is so important...but as I'm new here, and don't want to wear out my welcome with one of my first posts, much less be presumptuous by copying huge tracts directly to a post, I'll cut this short.
I've just started Selegeline, myself--after learning about it in my regular course of alternative therapy research on the web. I've been taking 30mg/day--one dose, morning...for three days now. I have quite a bit of anxiety to deal with, also--what I now realize is the "normal" ADD related anxiety which has been with me always, but now PTSD, as well as a pretty virulent agoraphobia. You could say I'm essentially a vibrating knot of hypervigilance 98% of the day, really, and have been so for around 6 years, to date. Though it's gradually getting better through some applied therapeutic techniques--meditation, visualization, cog, etc--it's improving pretty damn slowly. But the first day I took the Seleg.--within about 30-45 minutes, actually, it was as though my body, and more importantly, mind, had finally and suddenly remembered how to relax! Not a heavy, sedated feeling like benzos, by any means--but very natural. The change WAS undeniable, however, and huge. I'm not saying this is a typical reaction, of course--or that if anxiety's a problem for you Selegiline is sure to do the trick--I have a pretty unique "profile"--a long history of serious depression--but judging from the extant literature, it's long (for a drug these days) history of safety, and many benefits, Deprenyl sounds worth trying to me. My mind's really been more on-track, too. I'll keep posting updates to this board to let you know how it's going.
"Once the bird is named we become blind to the bird's beauty, seeing only the name"
09-10-05, 06:45 AM
Also, supplementation with DL-phenylalanine is reported to help with cognitive function without adding to the "speedy" quality of sympathomimetics, as Tyrosine tends to.
Vassopressin, usually referred to as a "nootropic", or smartdrug, plays a large part both in memory formation and recall--and can be bought online, usually as a nasal spray. While it's well nigh impossible to find, now, Desmopressin is essentially a molecular analogue. Some claim Desmopressin is better, but I disagree. (I've found an online source, actually, but I suppose it wouldn't be Kosher to list it here...)
"<BIG>Vasopressin in the mammalian brain:
the neurobiology of a mnemonic peptide</BIG>
Diaz Brinton R.
Department of Molecular Pharmacology and Toxicology,
USC Pharmaceutical Sciences Center,
Los Angeles, USA.
Prog Brain Res 1998;119:177-99</SMALL>
<BIG><BIG>W</BIG></BIG>e have sought to understand the mechanisms by which VP can enhance memory function and in the process determine whether VP fulfills the requirements for neurotransmitter status. The latter goal of proving the neurotransmitter status of VP has been achieved through our findings and the results of many of the scientists contributing to this volume. With respect to elucidating the mechanisms by which VP can enhance memory function, results of our work have shown that VP and its receptors are present in brain regions known to be involved in memory function, that release of VP is inhibited by a factor that inhibits memory function, that VP can significantly enhance the morphological complexity and outgrowth of neurons involved in memory function, that second messenger systems held to be involved in learning and memory, cyclic AMP and calcium signaling pathways, are potentiated and activated by VP, that electrophysiological models of memory function are induced by VP, and that when animals remember a learned association VP content in brain increases over time during the active phase of remembering."