Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The psychopathological status of 25 inpatients suffering from clinically definite multiple sclerosis (MS) according to Poser criteria was assessed by using standardized methods (Structured Clinical Interview for DSM-III-R, Inpatient Multidimensional Psychiatric Scale, Hamilton and Montgomery-Asberg Depression Rating Scales and the Structured Interview for the Diagnosis of Alzheimer Dementia and Dementias of other Aetiology (SIDAM). Magnetic resonance (MRT) (0.5 T; T2-weighted sequence) of the brain was analysed by measuring the ventricular brain ration (VBR), the area of the corpus callosum (CC) and the extension of hyperintense lesions of the brainstem, the temporal lobes and the brain at all. Six of 25 (24%) of these moderately disabled patients (mean Extended Disability Score (EDSS) 3.3) were diagnosed to suffer from depressive mood disorder (major depression or dysthymia); 2 were demented. In correlation analysis, depression was unrelated to age, gender, duration of illness, status of disability (EDSS) or the results of cognitive assessment. No relationship between the depression scores and the different MRT measures could be identified. The presence or absence of gadolinium enhancement was also uncorrelated to depressive symptoms. Fatigue as measured by the Fatigue Severity Scale was unrelated to depression or subcortical brain atrophy (increased VBR) but significantly correlated to the area of hyperintense MRT changes in brainstem and midbrain. Cognitive impairment (decreased SIDAM scores) was correlated to the total area of hyperintense MRT changes of the brain parenchyma. The type of clinical course (relapsing-remitting vs chronic progredient) was not found to influence the affective or cognitive state in our MS patient's sample.
 ...
PMID:Correlates of cognitive impairment and depressive mood disorder in multiple sclerosis. 817 61

While commonly administered in the neuropsychological assessment of dementia, the Wechsler Adult Intelligence Scale-Revised (WAIS-R) is excessively long (70-90 min) and difficult for many patients. The present study examined WAIS-R data from patients with clinically distinct dementing disorders, including those with Alzheimer's, Huntington's, and Parkinson's disease (N = 148). The profiles of performance of these three patient groups across subtests were remarkably similar, suggesting that the use of a short form would not result in the loss of clinically significant information. The validity of several published short forms was reviewed. Although all of these systematically over- or underestimated Full Scale IQ for these patients, after a scaling table revision the Kaufman (1990) form appears to provide an accurate estimate of IQ. The use of this short form is therefore recommended to minimize frustration and fatigue on the part of the patient, and to allow the inclusion of other tests critical to the evaluation of dementia within a single assessment session.
 ...
PMID:Assessment of intellectual function in dementing disorders: validity of WAIS-R short forms for patients with Alzheimer's, Huntington's, and Parkinson's disease. 827 33

In an acute trial, three different dosages (60, 300, and 600 micrograms) of the endocrinologically inert but behaviorally active corticotropin 4-9 (ACTH4-9) fragment ebiratide were given to three patients with clinically probable Alzheimer's disease and five patients with a major depressive episode who were psychomotorly retarded. The drug was given intravenously in a double-blind, placebo-controlled, crossover design, and cognitive as well as psychopathologic assessments were carried out predrug and postdrug treatment. In summary, no adverse effect of the ACTH fragment was detected. In this explorative study, none of the patients improved cognitively, as measured by neuropsychologic testing. However, all patients, regardless of underlying disorder, reported a decrease of the feeling of tiredness or loss of energy, respectively. They felt more vigorous and alert. This occurred after any of the three doses of ACTH4-9, but not after placebo. In concert with reports from other studies, it is concluded that the ACTH4-9 fragment ebiratide may have activating properties in humans. However, given acutely, it does not seem to have antidementia or antidepressive efficacy.
 ...
PMID:Behavioral effects of a synthetic corticotropin 4-9 analog in patients with depression and patients with Alzheimer's disease. 839 47

We study an Attractor Neural Network that stores natural concepts, organized in semantic classes. The concepts are represented by distributed patterns over a space of attributes, and are related by both semantic and episodic associations. While semantic relations are expressed through an hierarchical coding over the attribute space, episodic links are realized via specific synaptic projections. Due to dynamic thresholds expressing neuronal fatigue, the network's behavior is characterized by convergence toward the concept patterns on a short time scale, and by transitions between the various patterns on a longer time scale. In its baseline, undamaged state, the network manifests semantic, episodic, and random transitions, and demonstrates the phenomenon of priming. Modeling possible pathological changes, we have found that increasing the 'noise' level or the rate of neuronal fatigue decreases the frequency of semantic transitions. When neurons characterized by large synaptic connectivity are deleted, semantic transitions decay before the episodic ones, in accordance with the findings in patients with Alzheimer's disease.
 ...
PMID:A neural model of the dynamic activation of memory. 847 86

The number of AIDS patients over age 60 has risen steadily in the past decade. The number of transfusion-acquired AIDS cases probably has peaked--or will soon peak. Homosexual (or bisexual) behavior remains the predominant risk factor for AIDS until the seventh decade. Disease progression appears to be more rapid in the elderly, although the observed shorter survival time may result from a delay in diagnosis. Symptoms of HIV infection are often nonspecific, such as fatigue, anorexia, weight loss, and decreased physical and cognitive function. The five most common opportunistic infections in older HIV-infected patients are Pneumocystis carinii pneumonia, tuberculosis, Mycobacterium avium complex, herpes zoster, and cytomegalovirus. A number of features of HIV-related dementia may help to distinguish it from Alzheimer's disease.
 ...
PMID:HIV infection in older patients: when to suspect the unexpected. 850 Jul 75

A deficit in glucose uptake and a deposition of amyloid beta-peptide (A beta) each occur in vulnerable brain regions in Alzheimer's disease (AD). It is not known whether mechanistic links exist between A beta deposition and impaired glucose transport. We now report that A beta impairs glucose transport in cultured rat hippocampal and cortical neurons by a mechanism involving membrane lipid peroxidation. A beta impaired 3H-deoxy-glucose transport in a concentration-dependent manner and with a time course preceding neurodegeneration. The decrease in glucose transport was followed by a decrease in cellular ATP levels. Impairment of glucose transport, ATP depletion, and cell death were each prevented in cultures pretreated with antioxidants. Exposure to FeSO4, an established inducer of lipid peroxidation, also impaired glucose transport. Immunoprecipitation and Western blot analyses showed that exposure of cultures to A beta induced conjugation of 4-hydroxynonenal (HNE), an aldehydic product of lipid peroxidation, to the neuronal glucose transport protein GLUT3. HNE induced a concentration-dependent impairment of glucose transport and subsequent ATP depletion. Impaired glucose transport was not caused by a decreased energy demand in the neurons, because ouabain, which inhibits Na+/K(+)-ATPase activity and thereby reduces neuronal ATP hydrolysis rate, had little or no effect on glucose transport. Collectively, the data demonstrate that lipid peroxidation mediates A beta-induced impairment of glucose transport in neurons and suggest that this action of A beta may contribute to decreased glucose uptake and neuronal degeneration in AD.
 ...
PMID:Amyloid beta-peptide impairs glucose transport in hippocampal and cortical neurons: involvement of membrane lipid peroxidation. 899 59

Currently available as a dietary supplement, the pineal hormone melatonin is portrayed by the media as a formidable weapon against disease and aging. Accordingly, primary health care providers should be cognizant of which of its proposed uses are supported by biomedical research and which are, as yet, unproven. Melatonin entrains circadian rhythms and, thus, can treat jet lag, delayed sleep phase syndrome, and sleep disorders in the blind and in some neurologically impaired children. By virtue of its hypnotic effect, melatonin can mitigate insomnia in the elderly. Reductions in melatonin secretion have been associated with many disorders, including cardiovascular disease, Alzheimer's, diabetes, SIDS, and aging; however, melatonin's role in their etiology and/or pathophysiology is unproven. Preliminary studies suggest a possible adjuvant therapeutic role for melatonin in cancer therapy. Melatonin secretion is reduced by alcohol, caffeine, and some commonly prescribed drugs. Since tolerance, fatigue, and other side effects have been reported, melatonin use on consecutive nights should be avoided and only the lowest effective hypnotic dose should be taken.
 ...
PMID:Melatonin: media hype or therapeutic breakthrough? 905 17

A placebo-controlled crossover design, with each treatment period lasting 6 weeks, was used to investigate effects of dronabinol in 15 patients with a diagnosis of probable Alzhemer's disease who were refusing food. Eleven patients completed both study periods; one patient who died of a heart attack 2 weeks before the end of the study was also included in the analysis. The study was terminated in 3 patients: one developed a grand mal seizure and 2 developed serious intercurrent infections. Body weight of study subjects increased more during the dronabinol treatment than during the placebo periods. Dronabinol treatment decreased severity of disturbed behavior and this effect persisted during the placebo period in patients who received dronabinol first. Adverse reactions observed more commonly during the dronabinol treatment than during placebo periods included euphoria, somnolence and tiredness, but did not require discontinuation of therapy. These results indicate that dronabinol is a promising novel therapeutic agent which may be useful not only for treatment of anorexia but also to improve disturbed behavior in patients with Alzheimer's disease.
 ...
PMID:Effects of dronabinol on anorexia and disturbed behavior in patients with Alzheimer's disease. 930 69

The authors rated 137 outpatients with probable Alzheimer's disease (AD) on the Cornell Scale for Depression in Dementia (CSDD) as part of routine evaluation. Principal-factors analysis with varimax rotation resulted in a four-factor solution that accounted for 43.1% of the common variance. The four factors included general depression (lack of reactivity to pleasant events, poor self-esteem, pessimism, loss of interest, physical complaints, psychomotor retardation, sadness); rhythm disturbances (difficulty falling asleep, multiple night awakenings, early morning awakenings, weight loss, diurnal variation of mood); agitation/psychosis (agitation, mood-congruent delusions, suicide); and negative symptoms (appetite loss, weight loss, lack of energy, loss of interest, lack of reactivity to pleasant events). The observed factor structure showed moderate concordance with the five symptom clusters proposed in the original presentation of the CSDD.
 ...
PMID:The factor structure of the Cornell Scale for Depression in Dementia among probable Alzheimer's disease patients. 965 54

Many approaches have been undertaken to understand Alzheimer's disease (AD) but the heterogeneity of the etiologic factors makes it difficult to define the clinically most important factor determining the onset and progression of the disease. However, there is increasing evidence that the previously so-called "secondary factors" such as a disturbed glucose metabolism, oxidative stress and formation of "advanced glycation endproducts" (AGEs) and their interaction in a vicious cycle are also important for the onset and progression of AD. AGEs are protein modifications that contribute to the formation of the histopathological and biochemical hallmarks of AD: amyloid plaques, neurofibrillary tangles and activated microglia. Oxidative modifications are formed by a complex cascade of dehydration, oxidation and cyclisation reactions, subsequent to a non-enzymatic reaction of sugars with amino groups of proteins. Accumulation of AGE-crosslinked proteins throughout life is a general phenomenon of ageing. However, AGEs are more than just markers of ageing since they can also exert adverse biologic effects on tissues and cells, including the activation of intracellular signal transduction pathways, leading to the upregulation of cytokine and free radical production (oxidative stress). Oxidative stress is involved in various divergent events leading to cell damage, including an increase in membrane rigidity, DNA strand breaks and an impairment in glucose uptake. In addition, other age-related metabolic changes such as depletion of antioxidants or decreased energy production by a disturbed glucose metabolism diminish the ability of the cell to cope with the effects of radical-induced membrane, protein and DNA damage. With our improving understanding of the molecular basis for the clinical symptoms of dementia, it is hoped that the elucidation of the etiologic causes, particularly the positive feedback loops involving radical damage and a reduced glucose metabolism, will help to develop novel "neuroprotective" treatment strategies able to interrupt this vicious cycle of oxidative stress and energy shortage in AD.
 ...
PMID:Alzheimer's disease--synergistic effects of glucose deficit, oxidative stress and advanced glycation endproducts. 972 Sep 73


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>