Plasma N-POMC, ACTH and Cortisol Concentrations in a Psychogeriatric Population

1990 ◽  
Vol 156 (5) ◽  
pp. 676-679 ◽  
Author(s):  
A. Leake ◽  
B. G. Charlton ◽  
P. J. Lowry ◽  
S. Jackson ◽  
A. Fairbairn ◽  
...  

Elderly patients with depression and Alzheimer-type dementia (ATD) were compared with age-matched control subjects using a protocol which measured Cortisol, adrenocorticotrophic hormone (ACTH) and N-terminal pro-opiomelanocortin (N-POMC) to determine diurnal variation and the effect of dexamethasone administration. Depressed patients had significantly elevated Cortisol concentrations both before and after dexamethasone administration. Basal ACTH and N-POMC concentrations were normal in depressed patients but were both elevated, compared with controls, after dexamethasone. By contrast, in ATD patients, Cortisol was elevated only after dexamethasone, as was ACTH, but not N-POMC. This may imply that the pattern of secretion of POMC-derived peptides underlying increased Cortisol secretion is different in ATD from that in depression.

1993 ◽  
Vol 163 (2) ◽  
pp. 155-165 ◽  
Author(s):  
S. M. Curran ◽  
C. M. Murray ◽  
M. Van Beck ◽  
N. Dougall ◽  
R. E. O'Carroll ◽  
...  

The uptake, at rest, of 99mTc-exametazime into different brain regions was compared using SPECT for 20 elderly subjects with major depressive disorder, 20 with Alzheimer-type dementia, and 30 age-matched normal volunteers. Uptake was referred to calcarine-occipital cortex as a reference sensory area. Cross-sectional differences between the three groups were highly statistically significant, but reflected primarily the reductions in cortical uptake in the Alzheimer group. A detailed comparison of depressed patients and controls identified decrements in anterior cingulate, temporal and frontal cortex and in caudate and thalamus in men only. These decrements were correlated with impairment of performance on a trail-making task, but were also associated with continuing treatment with antidepressants or benzodiazepines. However, most depressed patients had quantitatively normal scans for posterior parietal association cortex, and this suggests that SPECT may find a limited role in the differential diagnosis of depression and dementia. The reduced brain function in some depressed patients may parallel the findings from studies of brain structure in elderly depressives; there was a weak association between good outcome at 6–18 months and increased tracer uptake in subcortical areas.


1993 ◽  
Vol 23 (1) ◽  
pp. 65-70 ◽  
Author(s):  
Dario Grossi ◽  
James T. Becker ◽  
Christine Smith ◽  
Luigi Trojano

SynopsisImmediate memory for visuospatial information was assessed in patients affected by Alzheimer-type dementia but with unimpaired visuo-perceptual functions. Patients were given two tasks: one was a traditional visuospatial memory task (Corsi's block tapping test), the second explored specifically immediate memory for visuospatial patterns. The experiment was conducted in two parallel groups of patients in Italy and the United States, each with its own appropriate sample of normal control subjects. Results showed a specific deficit of visual working memory in demented patients, even in a task in which control subjects achieved error-free performance. These data are interpreted in the light of the Working Memory Model, and suggest that in dementia the functions of the Visuospatial Scratchpad, unlike the functions of the verbal subsystems, may be impaired.


2014 ◽  
Vol 58 (11) ◽  
pp. 6471-6476 ◽  
Author(s):  
S. Flanagan ◽  
S. L. Minassian ◽  
D. Morris ◽  
R. Ponnuraj ◽  
T. C. Marbury ◽  
...  

ABSTRACTTwo open-label, single-dose, parallel-group studies were conducted to characterize the pharmacokinetics of the novel antibacterial tedizolid and the safety of tedizolid phosphate, its prodrug, in renally or hepatically impaired subjects. Tedizolid pharmacokinetics in subjects with severe renal impairment without dialysis support was compared with that of matched control subjects with normal renal function. Effects of hemodialysis on tedizolid pharmacokinetics were determined in a separate cohort of subjects undergoing long-term hemodialysis. Effects of hepatic impairment on tedizolid pharmacokinetics were determined in subjects with moderate or severe hepatic impairment and compared with those of matched control subjects with normal hepatic function. Each participant received a single oral (hepatic impairment) or intravenous (renal impairment) dose of tedizolid phosphate at 200 mg; hemodialysis subjects received two doses (separated by 7 days), before and after dialysis, in a crossover fashion. The pharmacokinetics of tedizolid was similar in subjects with severe renal impairment and controls (∼8% lower area under the concentration-time curve [AUC], with a nearly identical peak concentration) and in subjects undergoing hemodialysis before and after tedizolid phosphate administration (∼9% lower AUC, with a 15% higher peak concentration); <10% of the dose was removed during 4 h of hemodialysis. Tedizolid pharmacokinetics was only minimally altered in subjects with moderate or severe hepatic impairment; the AUC was increased approximately 22% and 34%, respectively, compared with that of subjects in the control group. Tedizolid phosphate was generally well tolerated in all participants. These results suggest that tedizolid phosphate dose adjustments are not necessary in patients with any degree of renal or hepatic impairment. (This study has been registered at ClinicalTrials.gov under registration numbers NCT01452828 [renal study] and NCT01431833 [hepatic study].)


1989 ◽  
Vol 1 (2) ◽  
pp. 135-143 ◽  
Author(s):  
Anastasios Georgotas ◽  
Robert E. McCue ◽  
Barry Reisberg ◽  
Steven H. Ferris ◽  
Narmada Nagachandran ◽  
...  

Seventy-eight nondemented elderly depressed patients underwent an extensive battery of cognitive tess both before and after seven weeks of treatment with nortriptyline, phenelzine, or placebo. Clinical and cognitive evaluations of the patients were under double-blind conditions. Response to treatment did not appear to significantly affect cognitive capacity; neither did treatment with an active substance as compared to placebo. In addition, the baseline level of cognitive functioning did not appear related to whether a patient responded to treatment. The authors conclude that under optimal conditions neither antidepressant produces measurable changes in the cognitive capacity of nondemented elderly patients.


1987 ◽  
Vol 150 (5) ◽  
pp. 674-681 ◽  
Author(s):  
J. E. Christie ◽  
L. J. Whalley ◽  
J. Bennie ◽  
H. Dick ◽  
I. M. Blackburn ◽  
...  

A systematic endocrine investigation in dementia, depression and control subjects showed that plasma growth hormone (GH) was higher in the morning and plasma TSH concentrations were higher throughout the day in Alzheimer-type dementia (ATD) than in age-matched depressed patients (MDD), and plasma TSH concentrations were also higher throughout the day in female ATD compared with age-matched female control subjects. The increased plasma TSH concentrations could not be due to reduced negative feedback because plasma T3, T4 and rT3 were in the normal range. Plasma concentrations of oestrogen-stimulated neurophysin (ESN) were lower throughout the day in ATD compared with MDD and controls and lower in the morning compared with other dementias. The high plasma GH and TSH concentrations in ATD may reflect the reduced hypothalamic content of somatostatin in ATD, and the reduced concentrations of ESN may reflect reduced cholinergic activity in ATD prain. These selective hormonal changes provide a useful diagnostic test for Alzheimer's disease.


2019 ◽  
Vol 9 ◽  
pp. 2235042X1985348 ◽  
Author(s):  
Katrine Løppenthin ◽  
Bente Appel Esbensen ◽  
Mikkel Østergaard ◽  
Rikke Ibsen ◽  
Jakob Kjellberg ◽  
...  

Objective: The aim of this study was to examine the prevalence of morbidity and mortality in patients with seropositive rheumatoid arthritis (RA). Methods: Data were obtained from national population-based registries in the period 1998–2009. Prior to the seropositive RA diagnosis (International Classification of Disorders 10th revision M05), we identified a total of 21,558 patients and 87,384 age- and sex-matched control subjects. Odds for morbidity were calculated before and after the RA diagnosis. We estimated the overall survival based on the Kaplan–Meier method. Results: Patients with RA had statistically significantly higher odds for a number of co-morbidities prior to the onset of RA including diseases of the musculoskeletal system (odds ratio (OR) 3.10, 95% confidence interval (CI) 3.00–3.21), diseases involving the immune system (OR 1.45, 95% CI 1.29–1.64), endocrine diseases (OR 1.09, 95% CI 1.01–1.17), diseases of the circulatory system (OR 1.08, 95% CI 1.03–1.14) and diseases of the respiratory system (OR 1.30, 95% CI 1.22–1.38), compared with age- and sex-matched control subjects. After the RA diagnosis, the same trend was seen with higher odds for the same co-morbidities. We found a 5-year survival of 80% (95% CI 78–81%) for patients with RA, while for control subjects it was 88% (95% CI 88–89%). Conclusion: Compared with age- and sex-matched controls, patients with seropositive RA have higher odds for several co-morbidities prior to and, particularly, after the diagnosis of RA. Furthermore, patients with RA have a lower overall survival compared with age- and sex-matched controls.


2013 ◽  
Vol 16 (8) ◽  
pp. 1745-1754 ◽  
Author(s):  
Moran Golan ◽  
Gabriel Schreiber ◽  
Sofia Avissar

Abstract β-Arrestins 1 and 2, cytosolic proteins known to mediate receptor desensitization, endocytosis and G protein-independent signalling, are post-translationally modified by ubiquitination regulating their ability to serve as adaptors and scaffolds. β-Arrestins were suggested to play a role in the pathophysiology of depression and in antidepressant mechanism of action. To determine whether a depressive episode or antidepressant treatment induce significant selective differences in β-arrestin 1 and 2 levels or their ubiquitination patterns in leucocytes of patients with depression, 46 outpatients diagnosed with a depressive episode were examined before and after 4-wk antidepressant treatment compared with age- and gender-matched control subjects. β-Arrestin levels were measured by immunoblotting using anti-arrestin antibodies. Ubiquitination of β-arrestins was measured using anti-ubiquitin antibodies followed by an immunoprecipitation step and immunoblotting using anti-arrestin antibodies. Antidepressants induced selective alterations in leucocyte β-arrestin 1 and 2 levels and ubiquitination. The levels of β-arrestin 1 and 2 and their ubiquitinated forms in leucocytes of yet untreated patients with depression were significantly decreased in a symptom severity correlated manner compared to control subjects. Antidepressants normalized β-arrestin 1 and 2 levels and uncovered novel differences between the two isoforms: (a) while antidepressants normalized ubiquitination of β-arrestin 1, ubiquination of β-arrestin 2 was unaffected; (b) while under antidepressants ubiquitination extent of β-arrestin 1 positively correlated with its level, an inverse picture of negative correlation was found between ubiquitination extent of β-arrestin 2 and its level. We conclude that antidepressants may serve as a tool to detect functional differences between the two β-arrestin isoforms and that through these differential effects antidepressants can induce specific alterations in alternative cellular signalling.


1959 ◽  
Vol 19 (4) ◽  
pp. 389-397 ◽  
Author(s):  
K. FOTHERBY ◽  
J. A. STRONG

SUMMARY The hourly excretion of total 17-oxosteroids, total 17-hydroxycorticosteroids, dehydroepiandrosterone, pregnanetriol and pregnanediol by six normal males has been measured before and after a short intravenous infusion of adrenocorticotrophic hormone (ACTH). The peak, in the amounts of the various steroids excreted, occurred 3–4 hr after the commencement of the infusion, and within 6 hr the steroids, produced as a result of the ACTH stimulation, were completely excreted. On most days the subjects excreted quite large amounts of steroids during the period 6·30 a.m. to 10 a.m. The diurnal variation, however, was often obscured by sudden changes in the amounts of steroids excreted.


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