A class of medications used in the treatment of alzheimer’s disease (the most common dementing illness in the elderly), other dementias (e.g., Lewy Body Dementia), myasthenia gravis, glaucoma, and anticholinergic poisoning. Acetylcholinesterase inhibitors retard the breakdown of the neurotransmitter acetylcholine, which may improve cognition. They are also believed to have an effect on peptide processing, neurotransmitter receptors, and ion channels.
A substance that inhibits acetylcholinesterase (AChE) and thus the breakdown of acetylcholine to acetate and choline.
Natural toxins with alkaloids as active components. They have been detected in several edible fruits and vegetables such as potatoes, eggplant, and tomatoes. The most potent inhibitor is found in the potato. It is a glycoalkaloid, solanine. The solanine concentration in the potato varies with the degree of maturity at harvest, the rate of nitrogen fertilization, storage conditions, greening by exposure to light, and by variety. Commercial potatoes have a solanine content of 2-15 mg/100 g fresh weight. Greening of potatoes may increase the solanine content to 80-100 mg/100 g fresh weight. Most of the alkaloid is concentrated in the skin and potato sprouts. It is generally accepted that a solanine content of 20 mg/100 g fresh weight is the upper safe limit of consumption. Potatoes also can contain other glycoalkaloids (chaconine and tomatine) with properties similar to solanine. The symptoms seen in potato poisoning may be due to the combined effects of these alkaloids. Potato poisoning is a very rare event and would require the consumption of enormous quantities of potatoes.
In the realm of therapeutics, there exists a cluster of medications employed for addressing the state of mild to moderate cognitive decline stemming from the insidious Alzheimer’s disease. This neurodegenerative condition manifests as an inadequacy in the neurotransmitter acetylcholine within the intricate confines of the human brain.
The mechanism of action of acetylcholinesterase inhibitors revolves around impeding the functionality of acetylcholinesterase, an enzyme dwelling within the confines of the cerebral region, entrusted with the responsibility of dismantling acetylcholine. This interference consequently gives rise to escalated levels of acetylcholine. Remarkably, in almost fifty percent of all patients, these medications exhibit the ability to decelerate the relentless advancement of dementia. It is important to note, however, that they bear no influence on dementia arising from alternative etiologies such as stroke or traumatic brain injury.
Frequently encountered adverse effects encompass sensations of nausea, dizziness, and headaches. In rare instances, there exists the potential for encountering challenges in the act of urination.