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My husband was diagnosed with moderate Alzheimer's disease in 2007. Since that time we have tried many medications that claimed to be effective in Alzheimer's treatment but in general they were useless. His condition was gradually getting worse and nothing really helped. About three months ago he started hallucinating and stopped recognizing the family members. It was unbearable to see him like that. So I asked our doctor to prescribe him with some new medication. We switched to Galantamine and it was pure luck! The hallucinations disappeared, memory came back and he started reacting better to things that used to confuse him before. I think this med is a god sent!

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I am a 55-year-old male with early-onset Alzheimer's disease. I have been on Galantamine for 4 months now and I've noticed considerable improvement in my condition. The feeling of a thick fog around me has disappeared and I can percept the reality like a normal person, without slow reactions and getting frozen. I have not noticed any side-effects at all after using Galantamine for this period of time. I am hopeful to see further changes for the better.

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Another interesting aspect of galantamine's mechanism of action is that in addition to increasing serum ACh, it also binds allosterically to nicotinic acetylcholine receptors (nAChR), potentiating their activity and therefore, counteracting the down-regulated receptors secondary to neuronal damage in AD 10.

The non-covalent interaction between edrophonium and cholinesterase is relatively short lived, lasting 2-10 minutes (Pappano, 2012).

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Using FDA-approved drugs for the treatment of AD in the model system of eyeblink classical conditioning in rabbits, we observed no synergy with combinations of memantine and galantamine or donepezil.

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Some older animal studies report narrowing of attention onto high-salience cues and compromised latent inhibition, but these results are challenged by more recent data indicating normal function.

This reduction of the renal functions causes accumulation of drugs such as lithium and rivastigmine in the body even with normal dosages, resulting in drug toxicity.

Language problems such as word-finding difficulty occurs early but impaired comprehension or decreased speech output may occur in the later stages.

Donepezil was recently approved to treat severe AD as well.

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Therefore, the dose of galantamine that attenuates nicotine reinforcement and reinstatement is likely to represent a clinically relevant dose in humans.

The quality of the evidence however is poor and the benefit is small.

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Since a higher dose of donepezil had an inhibitory effect on dopamine cell firing, these results argue in favor of the notion that galantamine increases dopamine cell firing through allosteric potentiation of nAChRs.

This is accounted for by the possible differences in their inactive ingredients such as color and flavor additives, and by the copyright and trademark regulations that does not allow for exact copies of the existing brand-name products.

Galantamine is a specific, competitive and reversible ChEI that was approved in Sweden in 2000.

Galantamine increases the concentration of acetylcholine (ACh) in brain tissue through competitive and reversible inhibition of its hydrolysis by acetylcholinesterase (AChE).

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Mindfulness during the day, and especially right before bed, is a great way to become more lucid during the night.

The mean plasma concentration-time profiles of galantamine were very similar after single doses of galantamine (4 and 8 mg), and there was an approximate dose proportionality of galantamine pharmacokinetic parameters in both Caucasian and Japanese ethnic groups.

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The prevalence of AD doubles every 5 years after the age of 60 years; therefore, by the age of 85 years, 30% of the population has AD.

Therefore they are limited in the information that can be provided about long-term effects in a chronic disease such as AD.

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Tentative conclusions from studies in normal subjects are that acute lithium does not affect short-term memory; subchronic administration spares basic short-term memory of ongoing events but higher task demands (as in neuropsychological testing) occasionally reveal mild deficits.

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Prior to 2003, a different study from 1985 had tested young, healthy adults, but this study had 12 subjects and used a short treatment period.

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