Theparasympathetic nervous system, which uses acetylcholine almost exclusively to send its messages, is said to be almost entirely cholinergic. Neuromuscular junctions, preganglionic neurons of thesympathetic nervous system, thebasal forebrain, and brain stem complexes are also cholinergic, as are the receptor for themerocrine sweat glands.
In neuroscience and related fields, the term cholinergic is used in these related contexts:
The hypothesis states that a possible cause of AD is the reduced synthesis ofacetylcholine, a neurotransmitter involved in both memory and learning, two important components of AD. Many current drug therapies for AD are centered on the cholinergic hypothesis, although not all have been effective. Studies performed in the 1980s demonstrated significant impairment of cholinergic markers in Alzheimer's patients.[4]
Thus it was proposed that degeneration of cholinergic neurons in the basal forebrain and the associated loss of cholinergic neurotransmission in the cerebral cortex and other areas contributed significantly to the deterioration in cognitive function seen in patients with Alzheimer's disease[5]
Further studies on the cholinergic system and AD demonstrated acetylcholine plays a role in learning and memory.Scopolamine, ananticholinergic drug, was used to block cholinergic activity in young adults and induce memory impairments similar to those present in the elderly. The memory impairments were reversed when treated withphysostigmine, a cholinergic agonist. However, reversing memory impairments in AD patients may not be this easy due to permanent changes in brain structure.[6]
When young adults perform memory and attention tasks, brain activation patterns are balanced between thefrontal andoccipital lobes, creating a balance betweenbottom-up and top-down processing. Normal cognitive aging may affect long term and working memory, though the cholinergic system andcortical areas maintain performance through functional compensation. Adults with AD presenting with dysfunction of the cholinergic system are not able to compensate for long-term and working memory deficits.[7]
AD is currently treated by increasing acetylcholine concentration by usingacetylcholinesterase inhibitors to inhibitacetylcholinesterase from breaking down acetylcholine. Current acetylcholinesterase inhibitors approved in the United States by the FDA to treat Alzheimer's includedonepezil,rivastigmine, andgalantamine. These drugs work to increase the levels of acetylcholine and subsequently increase the function of neural cells.[8] However, not all treatments based upon the cholinergic hypothesis have been successful in treating the symptoms or slowing the progression of AD.[9] Therefore, a disruption to the cholinergic system has been proposed as a consequence of AD rather than a direct cause.[8]
^Vardanyan, R.S.; Hruby, V.J. (2006). "Cholinomimetics".Synthesis of Essential Drugs. Elsevier. pp. 179–193.doi:10.1016/b978-044452166-8/50013-3.ISBN978-0-444-52166-8.Cholinomimetics or cholinergic drugs are those drugs that cause effects similar to those resulting from introduction of acetylcholine, or simulation of ganglions of the parasympathetic nervous system. These drugs imitate action of endogenously released acetylcholine.
