Common Drug Q&A » Alzheimers » Memantine


A: First, confirm that your primary care physician has diagnosed the underlying cause of your nystagmus.

Nystagmus is a clinical finding, not a disease. There are several different potential causes and underlying diseases, some very serious.
You don’t want to treat a symptom and ignore the cause.

Once the diagnosis and treatment have been addressed, if the nystagmus continues, ask your physician for a referral to a neurologist. They are best qualified to recommend treatment… and, yes, nerve modifies like Neurontin (gabapentin) may help. There are many other options.
Namenda (memantine) is still in trials for this use. It is unproven.

Q: social anexity, confidence, outgoing, medication, adderall, xanax, intunive, memantine?
Hi, Im currently a junor in highschool and all my life Ive had social anexity but never knew it until I was perscribed Adderall for my ADD, the first time I took adderall I didnt experence a “high” but I noticed that I was much more tollerant of annoying people, I was smileing at everyone, and the biggest thing was that I could make eye contact. I hadnt even realized what my teachers face actually looked like until that day because I guess I just dont make eye contact. But the down side was that this great effect faded quickly, I do not take my medication on the weekend to avoid developing dependence and reduce my tollerance, mondays back on the medication give me a little bit of those innital effects but not quite the same. I would like to know which of these options would be the best for me.
1 memantine – reduce tollerance to adderall and reduce GAD generalized anexity disorder
2 xanax – idk if it makes you outgoing or just reduces anexity, VERY Addictive i’ve heard, If i would chose this option i would only use this for concerts and other social situations where i cant really get involved with my friend because im overly shy.
3 intunive – new ADD medicine from the shire drug development also makes adderall. benefits its non stimulant and can be taken in congution with adderall so i could cycle from one to the other to reduce tollerance
4 some sort of anti depresant. i dont like the idea of an anti depresant because from my research ive found that it actually induces downregulation of dopamine, seratonin, etc. essentally it makes it so that you cant be as naturally happy after long term use.

This is a very big issue with me, If youre well read, and know what youre talking about or have personal experiences please share them with me I would really appriciate the help. My body and health is so important to me, Ive been doing an incredible amout of research about all functions of the brain, neuro trasmitters, you name it, ive studied it haha, I just would really like to feel how i felt with boosted confidence, positive mood, and comfortable talking to people face to face with eye contact. Sometimes when im walking down the hallways at school i check my phone or look up at the clock even if i dont care what time it is to avoide eye contact. on a good adderall day ive noticed that more people initate a conversation with me just because i seem happy and interested in them. If you dont have social anexity disorder please dont respond just by saying just smile more and look people in the eye, if you dont have SAD you probally dont understand the undescribable feeling you get when eye contact is established and youre forced to look away, its awful. I just want to use some sort of medicine as an aid until i get comfortable and my SAD goes away. thank you so much for reading this i cant wait to hear your answers!

A: i take nuvigil for ADD and to keep me alert and wake up
i also have BAD social anxiety, i used to take ativan for it but it made you forget things sometimes and it always seemed like you were out of it, kinda like a high

now im on xanax and i can talk to ANYone, its really simply amazing. ativan made me calm and quiet, xanax calms my anxiety AND makes me more outgoing

Q: What are the structures and events that are involved at the site where glutamate causes transmission…?
What are the structures and events that are involved at the site where glutamate causes transmission of an impulse between two neurons in the brain?

HOw can MK801 and memantine slow the growth of glioma?

Please help me with these questions and tell me any useful websites where I can find information because I really don’t get it, and can’ seem to find find anything on it in my textbook or on the internet.
Also some technologies taht could be used to study glial cancer
Also some technologies thatt could be used to study glial cancer

A: This is a tough one. I’ll do my best.

What are the structures and events that are involved at the site where glutamate causes transmission of an impulse between two neurons in the brain?

Glutamate is a neurotransmitter which is released from the axon terminal and binds with a surface receptor on an effector cell (such as another neuron). Astrocytes function to absorb glutamate and process by converting it to glutamine then delivering it back to the pre-synaptic cell.

Not sure the level of detail you need, but hopefully this gives you a starting point.

HOw can MK801 and memantine slow the growth of glioma?

MK801 and memantine are known glutamate antagonists, which bind with the glutamate receptor. Tumor cells in the brain (gliomas) have been found to release an excessive amount of glutamate into the brain extra-cellular matrix leading to neuronal cell death. These drugs apparently help to prevent neuronal death and possibly inhibit tumor growth by preventing glutamate release. Here is an excellent article, that I think answers your question directly and will probably be a better source for you than me:


Also some technologies thatt could be used to study glial cancer

I would guess the most effective would be conventional methods like genetics, various imaging methods (CT scans, PET scans, MRIs).

Q: NMDA receptor antagonists?
Why is it that activation of the NMDA receptor by glutamate is responsible for neuronal plasticity, memory and learning but NMDA receptor antagonists (such as memantine) are used in the treatment of Alzheimer’s disease? It seems that a perceived side effect of the NMDAR antagonist would be memory and learning deficits? Also, since NMDARs are responsible for excitotoxicity would it stand to reason that antagonists such as dexomethorphan dosed regularly might be effective in treating stroke victims, or those predisposed to schizophrenia? I have read an exhausting 16 hours about all of this and the potential for use of NMDAR antagonists in antinociception, potentiating opioids and mitigating withdrawal – plus antidepressant effects? Does glutamate play a role in depression and pain? Too many questions, I know, who is really, really smart- :-)

(note, this originally was errantly placed in biology section_

A: Memantine (sold in the USA as Namenda) is a moderate affinity antagonist of the NMDA receptor. The primary goal of this treatment is to limit excitotoxic injury due to calcium flux through the NMDA-R, which has some of the highest calcium permeabilities of any channel desribed. The compound also has a relatively rapid off-rate and it allows for the NMDA-R to still respond if glutamate concentrations are high enough.
Given the relatively modest effects of anticholinergic drugs in treating AD symptoms this was viewed as a way to mitigate the worsening of symptoms in later stage disease where it is felt that excitotoxicity may be playing a more important role.
Interstingly, memantine also has an impact at both cholinergic and serotonergic synapses which may likely confuse the issue somewhat.

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