Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Memory function in the aged is described as due to the interaction of a number of variables in addition to physiology, including affective state and environmental conditions. Depression can cause a series of behavioral patterns ranging from exaggeration of memory complaint, to simulation of organic dysfunction, to "pseudodementia" in which there is production of an actual organic mental syndrome. Stress and noxious environmental conditions also contribute to cognitive dysfunction. Custodial care is singled out as especially harmful, producing a form of "excess disability" termed "unorientation" in which apparently impaired memory results from an apathetic, withdrawn reaction to the environment. All these adaptational patterns are subject to prevention, modification, and in some cases, reversal.
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PMID:Adaptational factors in memory function in the aged. 36 90

Research on cognitive impairment in chronic alcoholics has generally focused on pathology associated with organic brain damage. On the other hand, deficits more typical of the functional psychoses have been less explored, due to the absence of appropriate tests. By using the Thought Disorder Rating Scale (TDRS) recently developed at our Center, however, we have tested chronic alcoholics for the presence of classical symptoms of thought disorder. This test is based on the assessment of the patient's verbal behavior by an experienced clinician. Twenty subjects free of psychosis, severe withdrawal symptoms, and medical illness were, after detoxification, administered a test battery which included the TDRS, the Bender-Gestalt Test, and the Zung Self-rating Depression Scale (SDS). Five scored pathologically for thought disorder and of them four had abnormal Benders; whereas only two of 15 of those without thought disorder had abnormal Benders (t = 2.84, p < .01). Although SDS scores for both groups were in the depressed range, there was no significant difference between SDS means for the two groups. TDRS scores for these alcoholics are compared with those for other diagnosed groups, and implications for future investigation are discussed.
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PMID:Thought disorder in alcoholics. 55 22

Recent research indicates a possible cholinergic involvement in memory processes and thus the possibility that acetylcholine deficiency may underlie memory impairment in senile dementia. Deanol (2-dimethylaminoethanol), which is assumed to increase brain acetylcholine, was given openly for 4 weeks to 14 senile outpatients, to determine the safety of the drug and whether or not it reduces cognitive impairment. The dosage was gradually increased to 600 mg three times daily during the first two weeks, with no adverse effects. Ten patients improved globally and 4 were unchanged (p less than .01). The total score on the Sandoz Clinical Assessment-Geriatric (SCAG) was lowered by the third week (p less than .01), primarily as a result of reduced depression, irritability and anxiety, and increased motivation-initiative. However, neither the clinical ratings nor an extensive pre- versus post-treatment series of cognitive tests revealed changes in memory or other cognitive functions. Since a similar separate study with a different compound produced no behavioral changes, it is unlikely that the improvement with deanol was due entirely to placebo effects. The results thus suggest that although deanol may not improve memory, it may produce positive behavioral changes in some senile patients.
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PMID:Senile dementia: treatment with deanol. 86 68

A distinct hypokinetic syndrome appears to exist across several different neuropsychiatric diagnoses, involving (1) slowed motor activity with difficulty initiating and sustaining behaviors, (2) anhedonia with depressed mood and reduced affective range, and (3) cognitive impairment. Specifically, three well-recognized states--parkinsonism, retarded depression, and the negative symptoms of schizophrenia--prominently feature the components of this syndrome, and reduced dopamine turnover in the brain has been hypothesized to play a part in the pathophysiology of each. While aspects of this conceptualization remain controversial, it generates testable hypotheses that could have implications for the understanding and treatment of these states.
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PMID:Akinesia: a syndrome common to parkinsonism, retarded depression, and negative symptoms of schizophrenia. 135 15

Somatostatin (somatotropin release-inhibiting factor, SRIF) was originally discovered (1) during the purification of growth hormone-releasing factor from rat hypothalamus and was subsequently isolated and characterized (2) in 1972 from ovine hypothalamus. Since its initial characterization, SRIF has been shown to fulfill criteria for a neurotransmitter and to directly modulate neuronal activity as well as acting as an inhibitory factor regulating endocrine and exocrine secretion. Alterations in cerebrospinal fluid (CSF) concentrations of SRIF have been reported in several diseases exhibiting prominent cognitive dysfunction, including Alzheimer's disease (AD), major depression, Huntington's chorea, multiple sclerosis, schizophrenia and Parkinson's disease, while evidence for regional brain tissue concentration deficits in SRIF are more specific for AD. This mini-review will focus on the studies reporting alterations in CSF and postmortem tissue concentrations of SRIF in AD and depression.
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PMID:Somatostatin in Alzheimer's disease and depression. 135 21

Moclobemide is a reversible and selective inhibitor of the enzyme monoamine oxidase (MAO) subtype A with a broad spectrum of antidepressant activity. Controlled clinical studies suggest that the short term clinical efficacy of moclobemide is significantly superior to that of placebo, and comparable to that of the tricyclic antidepressants clomipramine, amitriptyline, imipramine and desipramine, the irreversible MAO inhibitor tranylcypromine and the second-generation antidepressants maprotiline, mianserin and fluvoxamine in the treatment of major depressive illness. Moclobemide appears to be equally effective in endogenous and nonendogenous depression, producing marked amelioration of clinical features of psychomotor retardation and depressed mood. Moclobemide is well tolerated, being largely devoid of the anticholinergic adverse effects, symptomatic postural hypotension and weight gain variously associated with the tricyclic antidepressants and irreversible MAO inhibitors, and appears considerably safer on overdosage than the tricyclic and second generation antidepressants. Moreover, moclobemide offers the advantage over the older, irreversible MAO inhibitors of causing only minimal potentiation of the pressor response to dietary tyramine (the so-called 'cheese effect'). Consequently, the risk of potentially fatal hypertensive crisis, a major deterrent to the wider acceptance of these earlier compounds, is substantially reduced with moclobemide, and the need for dietary precautions is minimised. With its efficacy against endogenous and nonendogenous depression, relatively rapid onset of antidepressant activity, and absence of carry-over effects on treatment withdrawal, moclobemide is likely to make an important contribution to the treatment of major depressive illness. Its favourable tolerability profile, safety on overdosage and beneficial effect on age-related cognitive impairment may be of particular value in the elderly and those with concurrent physical illness.
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PMID:Moclobemide. A review of its pharmacological properties and therapeutic use in depressive illness. 137 19

1. In a multicenter, placebo-controlled, double-blind clinical trial in 156 elderly patients with psychopathologic symptoms, glycosaminoglycan polysulfate was found to be a therapeutically effective agent in the treatment of the earliest manifestations of a dementing process. 2. Treatment with glycosaminoglycan polysulfate in the daily dosage of 600 LRU, administered on the basis of a divided dosage schedule for 24 weeks, was significantly superior to an inactive placebo on several outcome measures including the SCAG Total and factor scores (i.e., Cognitive Dysfunction, Withdrawal, Agitation/Irritability and Depression), the NOWLIS Total and Fatiguability factor scores, the MMSE, the HAM-D Total and Vegetative Symptoms factor score and the CGI Severity of Illness and Global Improvement. 3. The drug was well tolerated; vital signs and laboratory measures did not show clinically significant changes within the experimental period.
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PMID:Early manifestations of dementing illness: treatment with glycosaminoglycan polysulfate. 137 39

The effects of cognitive-behavioral group therapy, focused visual imagery group therapy, and education-discussion groups on cognition, depression, hopelessness, and dissatisfaction with life were studied among depressed nursing home residents. Seventy-six depressed subjects with mild to moderate cognitive decline participated in nurse-led 24-week protocols. Data were collected 4 weeks before the interventions, 8 and 20 weeks after treatment initiation, and 4 weeks after treatment termination. There were no significant changes in depression, hopelessness, or life satisfaction scores for any of the three conditions. Participants in the cognitive-behavioral and focused visual imagery groups showed a significant improvement beginning 8 weeks after treatment initiation on cognitive scores. These findings are encouraging indications that cognitive-behavioral and focused visual imagery group therapies may reduce cognitive impairment in depressed nursing home residents with mild to moderate cognitive decline.
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PMID:Effects of group interventions on cognition and depression in nursing home residents. 138 47

The purpose of this study was to explore further the hypothesis that changes in cognitive function may occur in the mild stages of multiple sclerosis (MS) by determining whether ventricular enlargement was related to cognitive function. Ten measures of ventricular size were made in a sample of 123 MS patients with mild disability and 60 well-matched healthy controls. In addition, sixteen tests of cognitive function and the Beck Depression Inventory were administered. For the MS group, there were significant correlations between the ventricular measures and cognitive performance but not for the normal controls. Scores on the Beck Depression Inventory were not correlated with either cognitive performance or ventricular enlargement. These findings suggest that for the MS group cognitive impairment was related to the disease process but not to the level of depression.
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PMID:Ventricular size, cognitive function and depression in patients with multiple sclerosis. 139 45

Depression with cognitive impairment, so called depressive pseudodementia, is commonly mistaken for a neurodegenerative dementia. Using positron emission tomography (PET) derived measures of regional cerebral blood flow (rCBF) a cohort of 33 patients with major depression was studied. Ten patients displayed significant and reversible cognitive impairment. The patterns of rCBF of these patients were compared with a cohort of equally depressed non-cognitively impaired depressed patients. In the depressed cognitively impaired patients a profile of rCBF abnormalities was identified consisting of decreases in the left anterior medial prefrontal cortex and increases in the cerebellar vermis. These changes were additional to those seen in depression alone and are distinct from those described in neurodegenerative dementia. The cognitive impairment seen in a proportion of depressed patients would seem to be associated with dysfunction of neural systems distinct from those implicated in depression alone or the neurodegenerative dementias.
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PMID:Regional cerebral blood flow abnormalities in depressed patients with cognitive impairment. 140 66


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