Yeah, that’s clearer. Let me answer two ways.
1. So like I said above, most AD drugs are acetylcholinesterase inhibitors. Acetylcholine is a chemical found in the brain that’s important for learning and memory, and chemicals that end in -ase are almost always enzymes that degrade the thing in the first part of the name. So acetylcholine + (ester)ase = something that breaks down acetylcholine. An acetylcholinesterase gets rid of acetylcholine.
If you were a scientist and you wanted to figure out how to improve learning and memory, you might think, gee, since acetylcholine is important for learning and memory, if we could only stop acetylcholinesterase from breaking it down, maybe learning and memory would improve!
And that’s what an acetylcholinesterase inhibitor does. It stops acetylcholine from being broken down, and it looks like doing that can help learning and memory. That’s at least how scientists think it helps AD patients.
A few small studies have been done looking at how these drugs affect normal, healthy people. In one study, pilots who were older but not demented performed significantly better on tasks related to aviation when they took donepezil (Aricept), the most common AD medication (from the journal Neurology).
As far as I know, there is no evidence showing that these drugs induce AD or AD-like symptoms, and I cannot think of a plausible biological mechanism for that to happen, either.
2. The AD drug that you mentioned, Memantine (Namenda) works on a different system in the brain, the glutamate system. Glutamate is a hugely important neurotransmitter and is involved in nearly every circuit in your brain.
In order for glutamate molecules to do anything, they need to bind to a receptor. There are two types of receptors that glutamate can bind to: AMPA and NMDA.
This drug, Memantine, binds to NMDA receptors. This makes it harder for glutamate to act on the receptor, since something else (the drug) is in the way*. As you can probably guess, since glutamate acts all over the brain, the drug does too. So it has the potential for some very wide-spread side effects.
However, at the right dose, studies have shown that Memantine is reasonably well tolerated (Neuropharmacology). It’s only when you take really high doses that the side effects start to get really nutty. And that’s exactly what you saw with your mom.
After a quick search I couldn’t find any articles that look specifically at cognitive effects of Memantine on normal, healthy people. So I’ll have to just take a stab in the dark. I don’t see any reason why it would act differently in normal, healthy people vs AD patients. At low doses there are probably some but minimal side effects, and at high doses you probably go pretty nuts.
Since this is way too long already, I will stop here. But I want to reiterate what @sevenfourteen said above: AD diagnosis can’t be made until after death. The diagnostic criteria are based on specific biological markers. If you are worried that it is being overdiagnosed, definitely read up on how the diagnosis is made—I think you will be surprised.
Whew. Sorry. Hope the answer you were looking for is in there somewhere.
*this is a really oversimplified version of what actually happens at the receptor. If you’re interested I can explain more about what really happens—it’s not complicated, just takes a lot of steps to explain.