Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.7 (acetylcholinesterase)
 28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The plasma cholinesterase variants in 80 patients having Down's syndrome have been examined and compared with a random control sample of individuals domiciled in the same area. Neither a change in frequency of known C5+ variant nor any new variant has been found in the electrophoretic studies. A highly significant increase in frequency of the fluoride resistant gene as well as a significant decrease in frequency of the atypical gene has been found in the Down's syndrome individuals. This altered distribution of the rare phenotype of plasma cholinesterase in mental illness may lead to a useful diagnostic acid in genetic counselling.
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PMID:Plasma cholinesterase polymorphism in Down's syndrome. 13 57

The plasma cholinesterase variants of 190 mentally ill individuals having lithium prophylaxis have been examined. A significantly increased frequency of the E1f gene is reported. The effect of lithium nitrate and sodium nitrate on the plasma cholinesterase variants have been shown to be identical in the concentration range 25.0-50.0 mmol/l. The usual enzyme is slightly less sensitive to inhibition by either salt than the dibucaine resistant variant. The evidence suggest that the increased frequency of the E1f gene could be a genetic marker associated with some mental illness and not the result of lithium prophylaxis.
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PMID:Plasma cholinesterase variants in patients having lithium therapy. 85 31

A reference range for erythrocyte acetyl cholinesterase (EAChE) in 46 mentally normal subjects aged 65 years or over has been established. Previous reports of a relationship between changes in (EAChE) levels and mental illness (dementia and depression) in the elderly suggested that this determination may be useful in screening elderly subjects for these illnesses or as an aid to diagnostic classification. A study of normal and mentally ill elderly subjects in the community in Liverpool does not confirm a relationship with either senile dementia or depression and many of the changes in EAChE levels noted previously can be accounted for either by variations in the haematocrit or by a hitherto unreported lowering of EAChE levels in normal women over 80 years of age.
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PMID:Erythrocyte acetyl cholinesterase in elderly patients with dementia and depression compared with normal controls. 233 4

A monoclonal antibody raised against the receptor for nerve growth factor (NGF) has been used to map the distribution of NGF receptor-containing profiles within the human basal forebrain of four male and three female elderly patients without neurologic or psychiatric illness. Immunohistochemically processed tissue reveals a continuum of NGF receptor-positive neurons located within the medial septum, vertical and horizontal limb nuclei of the diagonal band, and nucleus basalis. NGF receptor-containing neurons are also found within the bed nucleus of the stria terminalis, the anterior commissure, the internal capsule, and the internal and external medullary laminae of the globus pallidus. Virtually all (greater than 95%) NGF receptor-containing neurons colocalize with the specific cholinergic marker choline acetyltransferase (ChAT) or the nonspecific marker acetylcholinesterase (AChE). Conversely, a few cholinergic perikarya are found which are not NGF receptor positive (and vice versa). These findings demonstrate that human basal forebrain neurons on which NGF receptor immunoreactivity is detected are primarily cholinergic and analogous to the nonhuman primate Ch1-Ch4 subgroups of Mesulam et al. (J. Comp. Neurol., 214:170-197, '83). NGF receptor-containing fiber tracts are observed emanating from the medial septum and vertical limb nucleus of the diagonal band coursing medially within the fornix. Another fascicle originating mainly from the nucleus basalis and travelling within the external capsule enroute to the cortex is observed innervating all cortical layers. Comparison of NGF receptor- and ChAT-containing neurons reveals cholinergic perikarya within the striatal complex, whereas virtually no NGF receptor-containing neurons are found in these structures. An occasional displaced NGF receptor-containing neurons is seen in the ventrolateral portion of the putamen and the white matter underlying the nucleus accumbens. These data are discussed in terms of the relationship of NGF receptor- and ChAT-containing neurons within the basal forebrain and in terms of the possible functional significance of NGF in normal and diseased brain.
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PMID:Nerve growth factor receptor immunoreactive profiles in the normal, aged human basal forebrain: colocalization with cholinergic neurons. 254 49

Patients who present with acute neuropsychiatric syndromes pose difficult diagnostic and treatment challenges. A history of psychiatric illness and treatment with psychotropic medication may be valuable clues to diagnosis and management of such patients. However, this information may also tempt a clinician to focus on a premature diagnosis, excluding other important possibilities. A case of a 42-year-old male with recurrent psychotic illness who developed an abrupt deterioration in mental and physical status is presented. Despite an initial good response to physostigmine, he was diagnosed with neuroleptic malignant syndrome and did not receive subsequent treatment with cholinesterase inhibitors. The patient expired within hours of arriving in the emergency room. The postmortem benztropine level was elevated, leading to the attribution of death to anticholinergic toxicity. This case serves to illustrate the difficulties in distinguishing features of anticholinergic toxicity and neuroleptic malignant syndrome.
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PMID:Anticholinergic toxicity masquerading as neuroleptic malignant syndrome: a case report and review. 764 37

In light of the recently reported neuropathologic and neurochemical abnormalities of the cholinergic pathways in autism, donepezil, a cholinesterase inhibitor, is a potentially useful agent in the treatment of cognitive and behavioral symptoms observed in this disorder. A retrospective pilot study was conducted to determine whether donepezil is effective in the treatment of children and adolescents with autism. Eight patients (mean age = 11.0 +/- 4.1 years; range 7-19 years) who met Diagnostic and Statistical Manual of Mental Disorders (4th edition) criteria for autistic disorder were openly treated with donepezil. All patients were on concomitant psychoactive medications. Four of these patients (50%) demonstrated significant improvement as assessed by the Aberrant Behavior Checklist and the Clinical Global Impression Scale. Decreases in the Irritability and Hyperactivity subscales were observed, but no changes in the Inappropriate Speech, Lethargy, and Stereotypies subscales were noted. Limited and transient side effects were reported, with one patient experiencing gastrointestinal disturbances and another reporting mild irritability. Double-blind, placebo-controlled investigations are needed to provide further evidence of the potential benefits of donepezil to patients with autistic disorder.
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PMID:A retrospective open trial of adjunctive donepezil in children and adolescents with autistic disorder. 1242 97

One of the more recently recognized problems in treatment of patients with Parkinson's disease (PD) is development of cognitive dysfunction and, in many cases, frank dementia. As patients with PD live longer, because of improved care and treatment of motor symptoms, dementia in PD is becoming a major contributor to morbidity in the illness. Prevalence studies suggest that up to 30% of patients with PD develop dementia. Dementia in PD patients is often a multifactorial condition. Neuropathologic changes caused by PD itself may cause memory loss. However, some patients with PD and memory decline also have pathologic changes that are more consistent with Alzheimer's disease. Many PD patients have a mix of the two types of pathology. Other factors, such as underlying illnesses, medication side effects, and interaction of therapeutic agents, may contribute to cognitive changes in PD patients. Predictors of development of dementia in PD include advancing age and severity of neurologic symptoms, which may interact with one another to produce this effect. Recent work suggests that tobacco use also may increase risk of PD dementia, despite its possible protective effect against development of PD itself. Presence of psychiatric illness, especially depression, may interfere with cognition and exacerbate memory loss. Reduction in the dose of dopaminergic agents and of other medications may be helpful in partially improving cognitive function in some cases. The balance between improvement of motor function and preservation of cognitive abilities must be weighed, and it is important for clinicians to discuss this trade-off with patients and their families. At this time, there is no US Food and Drug Administration-approved pharmacologic treatment for dementia in PD. However, medication used to treat Alzheimer's disease, such as acetylcholinesterase inhibitors, may slow progression of memory loss in some PD patients. Based on work from small double-blind studies, open-label trials, and case reports, cholinesterase inhibitors may be tried for treatment of dementia in PD, as long as the patient and caregivers understand that these agents are being used on an off-label basis. Surgical intervention, such as deep brain stimulation of the subthalamic nucleus or globus pallidus internus, although useful for treatment of motor symptoms in some PD patients, does not improve cognitive function in most cases and may actually worsen cognition in patients with pre-existing dementia. There is no specific exercise regimen or dietary guidelines for patients with PD who develop dementia. However, patients should be encouraged to lead a healthy lifestyle; this may improve overall well-being, which could impact positively on cognition function. Similarly, although assistive devices have not been developed for people with PD who have memory loss, any aid that increases mobility will probably improve mental and physical function. Clinicians should be mindful of the increased caregiver burden posed by PD patients who also have dementia. They should intervene appropriately to prevent caregiver distress and "burn out." Herbal and nutritional supplements have not been shown in clinical trials to be beneficial for treatment of any type of dementia, and thus are not recommended for PD patients with cognitive decline.
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PMID:Dementia in Parkinson's Disease. 1504 3

Psychiatric disorders are associated with autonomic dys-regulations. There is evidence that these dys-regulations are partly responsible for the increased mortality in patients with psychiatric disorders. The determination of the heart rate variability (HRV) is a method easily applicable and allows the assessment of the autonomic control of the heart rate regulation. A multitude of HRV parameters with different physiological meanings have been introduced, the most widely used parameters are presented and characterized in this paper. Many studies have shown a reduced HRV in patients with major depression. Most studies found a reduced parasympathetic activity. However some authors discuss an elevated sympathetic activity. The magnitude of HRV reduction correlates to the severity of the depression. In patients with coronary diseases, major depression is an independent risk factor of mortality. Antidepressive therapy with serotonin reuptake inhibitors has failed to improve the prognosis of this patients. Patients with panic disorders also have a reduced HRV due to an elevated sympathetic control and reduced vagal control. In schizophrenic patients a reduced HRV was found in long term electrocardiogram recordings, whereas short term recordings did not show a reduced HRV. Patients with Alzheimer's disease also have a reduced HRV, which is limited to the low frequency component. Therapy with cholinesterase inhibitors further influences HRV by reducing the high frequency component and might increase the risk for arrhythmias. HRV analysis and integration in the assessment and monitoring of psychiatric patients before and during therapy elucidate the role of autonomic disturbances in such diseases and may help to optimize treatment.
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PMID:[Heart and brain -- the influence of psychiatric disorders and their therapy on the heart rate variability]. 1580 37

Dementia is a mental disorder characterized by loss of intellectual ability sufficiently severe enough to interfere with one's occupational or social activities. Desmodium gangeticum commonly known as Salparni, is widely used in ayurveda for the treatment of neurological disorders. The present work was designed to assess the potential of aqueous extract of D. gangeticum (DG) as a nootropic agent in mice. DG (50, 100 and 200 mg/kg, p.o.) was administered for 7 successive days to both young and older mice. Exteroceptive behavioral models such as elevated plus maze and passive avoidance paradigm were employed to evaluate learning and memory. Scopolamine (0.4 mg/kg, i.p.) induced amnesia and ageing induced amnesia were the interoceptive behavioral models. To delineate the mechanism by which DG exerts nootropic activity, the effect of DG on whole brain AChE activity was also assessed. Piracetam (200 mg/kg, i.p.) was used as a standard nootropic agent. Pretreatment with DG (50, 100 and 200 mg/kg p.o.) for seven successive days significantly improved learning and memory in mice and reversed the amnesia induced by both, scopolamine (0.4 mg/kg, i.p.) and natural ageing. DG also decreased whole brain acetyl cholinesterase activity. Hence, D. gangeticum appears to be a promising candidate for improving memory and it would be worthwhile to explore the potential of this plant in the management of dementia and Alzheimer disease.
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PMID:Antiamnesic effects of Desmodium gangeticum in mice. 1694 93

Alzheimer's disease is a progressive neurological and psychiatric disorder. Oxidative stress and neuroinflammation have been implicated in pathophysiology of Alzheimer's disease. Inflammatory cells, such as astrocytes and microglia, are activated in areas of the brain affected by amyloid plaques and inflammatory mediators including cytokines, chemokines, prostaglandins, oxygen free radicals and reactive nitrogen species may have a crucial role in Alzheimer's disease pathogenesis. Central administration of colchicine, a microtubule-disrupting agent, causes loss of cholinergic neurons and cognitive dysfunction that is associated with excessive free radical generation. The present study was aimed to evaluate the effects of cyclooxygenase inhibitors against colchicine-induced cognitive dysfunction and oxidative stress in rats. Following intracerebroventricular (i.c.v.) administration of colchicine (15 microg/5 microl), rats exhibited poor retention of memory in Morris water maze and elevated plus maze task paradigms and oxidative stress in rats. Chronic treatment with naproxen (per se; 20 and 40 mg/kg, p.o.) or valdecoxib (per se; 5 and 10 mg/kg, p.o.) daily respectively for a period of 25 days beginning 4 days prior to colchicine injection significantly improved colchicine-induced cognitive impairment. Intracerebroventricular colchicine injection resulted in free radical generation characterized by alterations in oxidative stress markers with a significant increase in malondialdehyde and nitrite levels and depletion of reduced glutathione levels in the brains of rats. It also caused a decrease in acetylcholinesterase activity. Besides, improving cognitive dysfunction, chronic administration of cyclooxygenase inhibitors (naproxen and valdecoxib) significantly reduced elevated malondialdehyde, nitrite levels and restored reduced glutathione levels and acetylcholinesterase activity. The results of the present study indicated that naproxen (per se; 20 and 40 mg/kg, p.o.) or valdecoxib (per se; 5 and 10 mg/kg, p.o.) treatment has a neuroprotective role against colchicine-induced cognitive impairment and associated oxidative stress. The present findings further support the potential use of cyclooxygenase inhibitors in treatment of neurodegenerative diseases such as Alzheimer's disease.
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PMID:Differential effects of cyclooxygenase inhibitors on intracerebroventricular colchicine-induced dysfunction and oxidative stress in rats. 1702 65


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