Cognitive function acetylcholine

Sarter, M. Bruno, J. P. (1997). Cognitive functions of cortical acetylcholine toward a unifying hypothesis. Brain Res. Rev. 23, 28-46. 

Levin ED, Simon BB. (1998). Nicotinic acetylcholine involvement in cognitive function in animals. Psychopharmacology (Berlin). 138(3-4) 217-30. 

Arnsten, A.F.T. and van Dyck, C.H. (1997) Monoamine and acetylcholine influences on higher cognitive functions in nonhuman primates relevance to the treatment of Alzheimer s disease. In Brioni, J.D. and Decker, M.W., eds. Pharmacological Treatment of Alzheimer s Disease Molecular and Neurobiological Foundations. New York John Wiley Sons, pp. 63-86. 

A number of pathways contain acetylcholine, including neurons in the neostriatum, the medial septal nucleus, and the reticular formation. Cholinergic pathways appear to play an important role in cognitive functions, especially memory. Presenile dementia of the Alzheimer type is reportedly associated with a profound loss of cholinergic neurons. However, the specificity of this loss has been questioned because the levels of other putative transmitters, eg, somatostatin, are also decreased. 

Q6 Cholinesterase inhibitors block the action of the enzyme acetylcholinesterase (which normally hydrolyses acetylcholine) and so terminate its activity. These drugs increase the life of released acetylcholine at the synapse, leading to an enhancement of acetylcholine activity. Drug treatment for Alzheimer s disease is supervised in specialist clinics where the patient s cognitive function can be assessed at approximately three-monthly intervals. About half the patients treated show a decreased rate of cognitive decline while receiving this type of drug. 

It might be expected that the above structure should give rise to a bioantioxidant with an anticholineesterase activity. Indeed, anticholineesterase compounds are the most efficient up-to-date therapeutic agents applied for the Altzheimer s disease (AD) they make it possible to maintain the level of acetylcholine (responsible for memory and cognitive functions) in the disease-affected sections of brain. On the other hand, the oxidative stress, i.e., promotion of LPO in cell membranes of brain and in cells of peripheral systems and organs plays an important role in the development of AD [73]. 

There is some evidence that the availability of choline may be limiting for the synthesis of acetylcholine in the central nervous system under some conditions, and supplements of phosphatidylcholine increase the rate of acetylcholine turnover. One systematic review concludes that phosphatidylcholine supplements result in some improvement in cognitive function in patients with dementia, especially when this is secondary to cerebrovascular disorder (Fioravanti and Yanagi, 2000), but another concludes that there is no evidence to support its use in the treatment of dementia (Higgins and Flicker, 2000). Although phosphatidylcholine has been used to treat tardive dyskinesia... 

Repeated or long-term exposure to low levels of nerve agents can cause neurophysiological and behavioral alterations due to down-regulation of muscarinic receptors in the hippocampus as a reaction to acetylcholine accumulation at muscarinic receptor sites based on AChE inhibition. This phenomenon is considered to be the cause of behavior performance deficits, especially disruption of cognitive functions. 

Alzheimer s disease is characterized by a progressive impairment of cognitive functions including the loss of memory and the inability to perform basic daily life (56). Based on the cholinergic hypothesis, these symptoms are the results of the reduction in brain acetylcholine activity due to the catabolism of acetylcholine by ACHE (57). 

The arborvitae seed improves cognitive function and a7-nicotinic acetylcholine receptor (a7nAChR) protein expression in the hippocampus on AD model rats [195]. 

---