L-tryptophan and depressive illness

1972 ◽  
Vol 10 (19) ◽  
pp. 75-76
Keyword(s):  
Depressive Symptoms ◽  
Depressive Illness ◽  
Accurate Prediction ◽  
Psychiatric Clinic ◽  
Contributory Factor ◽  
Detailed Knowledge ◽  
Depressed Patients ◽  
The Brain ◽  
Low Rate

Some drugs which lower the concentration of amines in brain may produce depressive symptoms in man. An example of such a drug is reserpine which has been shown to lower the concentration of 5-hydroxytryptamine (5HT) in the brain.1 Recent studies of depressive illnesses suggest that, in some depressed patients, the cerebral content of 5HT (as reflected by CSF metabolites) is low, probably due more to a low rate of synthesis2 than to increased degradation.3 If reduced brain-5HT is a contributory factor in some depressive illnesses, restoring normal concentrations by promoting synthesis or reducing degradation should ameliorate the illness. However, evidence inconsistent with this hypothesis already exists.4 Furthermore, lack of detailed knowledge of the function of 5HT in the neurones which contain it makes accurate prediction from the animal laboratory to the psychiatric clinic difficult.

Tryptamine Metabolism in Depression

1965 ◽  
Vol 111 (479) ◽  
pp. 993-998 ◽  
Author(s):  
A. Coppen ◽  
D. M. Shaw ◽  
A. Malleson ◽  
E. Eccleston ◽  
G. Gundy
Keyword(s):  
Body Weight ◽  
Monoamine Oxidase ◽  
Previous Investigation ◽  
Monoamine Oxidase Inhibitor ◽  
Depressive Illness ◽  
Oxidase Inhibitor ◽  
Tryptophan Metabolism ◽  
Depressed Patients ◽  
Brain Amines ◽  
The Brain

In a previous investigation we showed that large doses of DL-tryptophan (214 mg./kg. body weight) given to depressed patients receiving tranylcypromine (a monoamine oxidase inhibitor) potentiated the antidepressive effects of the drug (Coppen, Shaw and Farrell, 1963). This procedure increases the level of brain 5-hydroxytryptamine (5 HT) and tryptamine in the rat (Hess and Doepfner, 1961). Reserpine reduces the level of these amines in the brain, and it is known that patients being treated for hypertension with this drug often become depressed. Thus there is evidence that increasing certain brain amines may alleviate, and depleting brain amines may induce, a depressive illness. We therefore decided to study tryptophan metabolism in depressed patients. The pathways with which we were concerned are shown below.

The Effects of Small Electrical Currents upon Depressive Symptoms

1974 ◽  
Vol 125 (587) ◽  
pp. 414-415 ◽  
Author(s):  
D. K. B. Nias ◽  
M. B. Shapiro
Keyword(s):  
Depressive Symptoms ◽  
Psychological Effects ◽  
Electrical Currents ◽  
Positive Current ◽  
Depressed Patients ◽  
Negative Current ◽  
The Brain

Lippold and Redfearn (1964) reported psychological effects from sending small direct electrical currents through the brain (polarization). For 26 subjects they found that scalp-positive current caused ‘alertness or more involvement in the environment’, whereas scalp-negative current caused ‘quietness and withdrawal’ (p. 771). Three other subjects reliably produced opposite changes. The observations were made during brief talks by judges unaware of the kind of current being administered. The present study, details of which are given by Nias (1968), aimed to observe the effects of polarization upon symptoms of depressed patients.

Tryptophan Pyrrolase—A Biochemical Factor in Depressive Illness?

1969 ◽  
Vol 115 (529) ◽  
pp. 1367-1374 ◽  
Author(s):  
G. Curzon
Keyword(s):  
Cerebrospinal Fluid ◽  
Acetic Acid ◽  
Depressive Symptoms ◽  
Direct Evidence ◽  
Severe Depression ◽  
Depressive Illness ◽  
Depressed Patients ◽  
Biochemical Factor ◽  
Tryptophan Pyrrolase ◽  
Lumbar Cerebrospinal Fluid

Reserpine, which depletes brain amines, not infrequently causes depression (Bunney and Davis, 1965), whereas monoamine oxidase inhibitors (MAOI) which raise brain amine levels (Maclean et al., 1965) may alleviate depressive symptoms. The alleviation has been reported to be enhanced by tryptophan (Coppen et al., 1967), which is a precursor of the amines 5-hydroxytryptamine (5HT) and tryptamine. The apparent prophylaxis by tryptophan of an annual episode of depression has also been reported (Hertz and Sulman, 1968). These findings suggest that elevation of one or both of the above amines is responsible for the therapeutic effect of MAOI, and that their insufficiency may be responsible for symptoms of the disease. Defective 5HT synthesis in depressive illness is indicated by a number of findings. (1) Depressed patients responding to the MAOI drug iproniazid were found in two studies (Pare and Sandier, 1959; Praag and Leijnse, 1963), though not in a third (Burgermeister et al., 1963), to have a lower initial urinary excretion of the 5HT metabolite 5-hydroxyindole acetic acid (5HIAA) than those who did not respond. (2) Depressed patients have a low content of 5HIAA in the lumbar cerebrospinal fluid (Ashcroft et al., 1966), which rises on recovery. Although work using animals (Guldberg and Yates, 1968; Eccleston et al., 1968) shows that changes in brain 5HT are paralleled by changes of 5HIAA in the CSF, the significance of this result is not altogether clear, as lumbar 5HIAA depends not only on brain 5HT metabolism but also on 5HIAA transport within the CSF (Ashcroft et al., 1966). Furthermore, a small group of acute schizophrenics on phenothiazines also had low 5HIAA. (3) There is some direct evidence of low 5HT (Shaw et al., 1967) or 5HIAA (Bourne et al., 1968) in the hindbrains of depressive suicides. (4) While single doses of 5-hydroxytryptophan, the immediate precursor of 5HT, do not alleviate depression, the remission of a prolonged episode of severe depression by administration of 5-hydroxytryptophan for five days has been reported (Persson and Roos, 1967).

Do nomifensine and low-dose flupenthixol differ from other antidepressive drugs?

1978 ◽  
Vol 16 (11) ◽  
pp. 43-44
Keyword(s):  
Depressive Symptoms ◽  
Low Dose ◽  
Psychomotor Retardation ◽  
Physiological Change ◽  
Depressed Patients ◽  
Antidepressive Drugs ◽  
Postsynaptic Site ◽  
Dopaminergic Pathways ◽  
The Brain

Some patients develop depressive symptoms when treated with reserpine1 2 or tetrabenazine,3 which deplete the brain of the three monoamines, dopamine, noradrenaline and 5-hydroxytryptamine (serotonin). Thus, defective transmission in some central noradrenergic or serotonergic pathways has been invoked as the possible physiological change underlying depressive symptoms. In line with this hypothesis, most effective anti-depressive drugs (e. g. amitriptyline and imipramine) block the re-uptake of one or more monoamines (including dopamine to some extent) and may thus potentiate transmission in these pathways. Most attention has focused on noradrenaline and serotonin. Studies of dopamine, however,4 indicate that its turnover may be reduced, particularly in depressed patients with marked psychomotor retardation. Since ascending dopaminergic pathways may function as components of the central mechanisms of reward5 and depressed patients gain little satisfaction from life, it is plausible that a lack of dopamine at the postsynaptic site may be associated with some depressions, or some particular features of depression.

scholarly journals Phosphodiesterase 8A to discriminate in blood samples depressed patients and suicide attempters from healthy controls based on A-to-I RNA editing modifications

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Nicolas Salvetat ◽  
Fabrice Chimienti ◽  
Christopher Cayzac ◽  
Benjamin Dubuc ◽  
Francisco Checa-Robles ◽  
...  
Keyword(s):  
Major Depressive Disorder ◽  
Depressive Disorder ◽  
Rna Editing ◽  
Whole Blood ◽  
Healthy Controls ◽  
Major Depressive ◽  
Suicide Attempters ◽  
Blood Samples ◽  
Depressed Patients ◽  
The Brain

AbstractMental health issues, including major depressive disorder, which can lead to suicidal behavior, are considered by the World Health Organization as a major threat to global health. Alterations in neurotransmitter signaling, e.g., serotonin and glutamate, or inflammatory response have been linked to both MDD and suicide. Phosphodiesterase 8A (PDE8A) gene expression is significantly decreased in the temporal cortex of major depressive disorder (MDD) patients. PDE8A specifically hydrolyzes adenosine 3′,5′-cyclic monophosphate (cAMP), which is a key second messenger involved in inflammation, cognition, and chronic antidepressant treatment. Moreover, alterations of RNA editing in PDE8A mRNA has been described in the brain of depressed suicide decedents. Here, we investigated PDE8A A-to-I RNA editing-related modifications in whole blood of depressed patients and suicide attempters compared to age-matched and sex-matched healthy controls. We report significant alterations of RNA editing of PDE8A in the blood of depressed patients and suicide attempters with major depression, for which the suicide attempt took place during the last month before sample collection. The reported RNA editing modifications in whole blood were similar to the changes observed in the brain of suicide decedents. Furthermore, analysis and combinations of different edited isoforms allowed us to discriminate between suicide attempters and control groups. Altogether, our results identify PDE8A as an immune response-related marker whose RNA editing modifications translate from brain to blood, suggesting that monitoring RNA editing in PDE8A in blood samples could help to evaluate depressive state and suicide risk.

Neuropsychological impairment in patients with major depressive disorder: the effects of feedback on task performance

2003 ◽  
Vol 33 (3) ◽  
pp. 455-467 ◽  
Author(s):  
F. C. MURPHY ◽  
A. MICHAEL ◽  
T. W. ROBBINS ◽  
B. J. SAHAKIAN
Keyword(s):  
Working Memory ◽  
Negative Feedback ◽  
Performance Feedback ◽  
Visual Discrimination ◽  
Negative Reinforcement ◽  
Spatial Working Memory ◽  
Memory Task ◽  
Depressive Illness ◽  
Reversal Task ◽  
Depressed Patients

Background. Recent evidence suggests that an abnormal response to performance feedback may contribute to the wide-ranging neuropsychological deficits typically associated with depressive illness. The present research sought to determine whether the inability of depressed patients to utilize performance feedback advantageously is equally true for accurate and misleading feedback.Method. Patients with major depression and matched controls completed: (1) a visual discrimination and reversal task that featured intermittent and misleading negative feedback; and (2) feedback and no-feedback versions of a computerised test of spatial working memory. In the feedback version, negative feedback was accurate, highly informative, and could be used as a mnemonic aid.Results. On the Probability Reversal task, depressed patients were impaired in their ability to maintain response set in the face of misleading negative feedback as shown by their increased tendency to switch responding to the ‘incorrect’ stimulus following negative reinforcement, relative to that of controls. Patients' ability to acquire and reverse the necessary visual discrimination was unimpaired. On the Spatial Working Memory task, depressed patients made significantly more between-search errors than controls on the most difficult trials, but their ability to use negative feedback to facilitate performance remained intact.Conclusions. The present results suggest that feedback can have different effects in different contexts. Misleading, negative feedback appears to disrupt the performance of depressed patients, whereas negative but accurate feedback does not. These findings are considered in the context of recent studies on reinforcement systems and their associated neurobiological substrates.

scholarly journals Agomelatine Increases BDNF Serum Levels in Depressed Patients in Correlation with the Improvement of Depressive Symptoms

2016 ◽  
Vol 19 (5) ◽  
pp. pyw003 ◽  
Author(s):  
Giovanni Martinotti ◽  
Mauro Pettorruso ◽  
Domenico De Berardis ◽  
Paola Annunziata Varasano ◽  
Gabriella Lucidi Pressanti ◽  
...  
Keyword(s):  
Depressive Symptoms ◽  
Serum Levels ◽  
Depressed Patients

Depressive Disorder in Primary Care

1987 ◽  
Vol 150 (6) ◽  
pp. 737-751 ◽  
Author(s):  
C. V. R. Blacker ◽  
A. W. Clare
Keyword(s):  
Primary Care ◽  
Depressive Symptoms ◽  
Depressive Disorders ◽  
Psychiatric Morbidity ◽  
Depressive Illness ◽  
Psychiatric Disturbance ◽  
Collaborative Studies ◽  
Effect Of Treatment ◽  
Precise Relationship ◽  
The Relationship

Since the pioneering study of psychiatric morbidity in primary care by Shepherdet alin 1966, it has become increasingly apparent that a substantial proportion (between 20% and 25%) of patients consulting their GP are suffering from some form of psychiatric disturbance (Goldberg & Blackwell, 1970; Hoeperet al,1979). The composition of this psychiatric morbidity has been shown to be almost wholly affective in nature and largely mild in degree. In their important review Jenkins & Shepherd (1983) recently summarised the now extensive findings relating to overall minor psychiatric morbidity in primary care. However, recent collaborative studies between psychiatrists and GPs have identified that within this dilute pool of minor disorders, lurks a significant but poorly served population of patients suffering from depressive disorders which are by no means minor in degree. A number of crucial issues regarding this depression in primary care emerge which the present paper aims to review. In particular, how common is it, and how severe? How does it present and what, if any, are its special characteristics? What is the precise relationship between depressive symptoms and depressive illness presenting to the GP and what is the relationship between physical illness and depression? And finally, what is the course and outcome of depression in this setting and what are the indications for and effect of treatment?

Depression in Geriatric Inpatients: Correlations with Nutritional State and Cognitive Functions

2016 ◽  
Vol 33 (S1) ◽  
pp. S472-S472
Author(s):  
I. Bonfitto ◽  
G. Moniello ◽  
L. Ariano ◽  
M. Pascucci ◽  
M.D. Zanasi ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Depressive Symptoms ◽  
Nutritional Status ◽  
Rating Scale ◽  
Assessment Tool ◽  
Mini Nutritional Assessment ◽  
Average Score ◽  
Depressed Patients ◽  
Increased Risk ◽  
Geriatric Inpatients

BackgroundAlthough the prevalence of malnutrition is relatively low among elderly people, the risk increases significantly among inpatients and even more in those with mental deterioration.AimsTo evaluate the possible association between the severity of depressive symptoms, the nutritional status and the cognitive decline in a sample of geriatric inpatients.MethodsFifty-one geriatric inpatients completed the following tests:– Hamilton Depression Rating Scale (HAM-D), to assess the severity of depressive symptoms;– Mini Nutritional Assessment (MNA), as a nutrition screening and assessment tool;– Mini Mental State Examination (MMSE), to assess the cognitive impairment.ResultsThere is a negative proportional relationship between HAM-D and MMSE scores (P = 0.001) and between HAM-D and MNA scores (P = 0.023). Depressed patients found to have a greater cognitive impairment and a worse nutritional status. Considering a HAM-D cut-off point of 14, distinguishing mild than moderate depression, it shows a significant correlation with the MNA scores (P = 0.008). Patients with HAM-D scores ≥ 14 have an average MNA score of 19.8, while patients with HAM-D scores < 14 have an MNA average score of 23.6. Euthymic or mildly depressed patients are not at risk of malnutrition, while those with moderate or severe depression have an increased risk of malnutrition.ConclusionsOur study shows significant correlations between the severity of depressive symptoms and the risk of malnutrition or cognitive impairment. A mild depression state does not seem to be associated with an increased risk of malnutrition.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Early Parent Death and the Clinical Scales of the MMPI

1978 ◽  
Vol 132 (6) ◽  
pp. 574-579 ◽  
Author(s):  
John Birtchnell
Keyword(s):  
Depressive Illness ◽  
Parent Death ◽  
Clinical Scales ◽  
Depressed Patients ◽  
Early Parent ◽  
Father Death ◽  
Age And Sex

There is growing evidence that early parent death can affect the severity of adult depressive illness. It was anticipated, therefore, that early-bereaved depressed patients might score higher on certain MMPI clinical scales than non-bereaved, depressed controls matched for age and sex. This is shown to be the case, the most affected scales being Hypochondriasis and Paranoia. Hypochondriasis is shown to be more strongly associated with early father death, while Paranoia is associated equally with mother and father death. There is some suggestion that early mother death is also associated with elevation of the F score. Early parent death is shown to have no effect upon the MMPI scores of non-depressed patients.

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