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

Attention deficit hyperactivity disorder (ADHD) is a chronic behavioral disorder characterized by persistent hyperactivity, impulsivity, and inattention that impairs educational achievement and/or social functioning. Its diagnosis is made by ascertaining whether the child's specific behaviors meet the diagnostic and statistical manual of mental disorders-IV-revised criteria. Its etiology is still unclear but recent studies suggest that genetics plays a major role in conferring susceptibility. Comorbidity with psychiatric disorders such as anxiety disorder, depression, oppositional defiant disorder and conduct disorder; and with specific learning disability is not uncommon. Although medication works well in most cases of ADHD, optimal treatment requires integrated medical and behavioral treatment. Methylphenidate (MPH) and atomoxetine are the two drugs being currently prescribed and their efficacy in decreasing the symptoms of ADHD is well documented. Pyschoeducational interventions in school can help increase the successful functioning of affected children and improve their academic performance. Almost half of affected children continue to show significant symptoms of the disorder into adolescence and young adulthood. The family physician can play an important role in detecting this condition early, coordinating its assessment and treatment, counseling the parents and classroom teacher, and monitoring the child's academic and psychosocial progress on a long-term basis.
 ...
PMID:Attention deficit hyperactivity disorder--a review for family physicians. 1638 76

Synucleinopathies, with and without dementia, encompass a wide range of diseases including Parkinson's disease, multiple system atrophy, rapid eye movement (REM) sleep behavior disorder, and dementia with Lewy bodies (DLB). DLB is a neurodegenerative disorder resulting in slowly progressive and unrelenting dementia until death. Prevalence studies suggest that it is the second most common dementing illness in the elderly. The neuropathologic findings of DLB show a wide anatomic range. Lewy bodies and Lewy-related pathology are found from the brain stem to the cortex and, in many cases, associated with concurrent Alzheimer's disease pathology. A recent international consortium on DLB has resulted in revised criteria for the clinical and pathological diagnosis of DLB incorporating new information about the core clinical features and improved methods for their assessment. The presentation of DLB is typically one of cortical and subcortical cognitive impairments, with worse visuospatial and executive dysfunction than Alzheimer's disease. There may be relative sparing of memory especially in the early stages. Core clinical features of DLB include fluctuating attention, recurrent visual hallucinations, and parkinsonism. Suggestive features include REM sleep behavior disorder, severe neuroleptic sensitivity, and low dopamine transporter uptake in the basal ganglia on functional neuroimaging. Additional supportive features that commonly occur in DLB, but with lower specificity, include repeated falls and syncope, transient, unexplained loss of consciousness, severe autonomic dysfunction, hallucinations in other modalities, systematized delusions, depression, relative preservation of medial temporal lobe structures on structural neuroimaging, reduced occipital activity on functional neuroimaging, prominent slow wave activity on electroencephalogram, and low uptake myocardial scintigraphy. Management of DLB includes pharmacological and nonpharmacological interventions for its cognitive, neuropsychiatric, motor, and sleep disturbances.
 ...
PMID:Dementia with Lewy bodies. 1722 40

This article examines coocurrence of three types of problems of adaptation during adolescence : abuse of psychotropic drugs, behavioral disorder (oppositional and behavioral disorders) and feelings of depression (depression and dysthymia). The study also examines behavioral, social as well as family characteristics which, during childhood, distinguish youths with many adaptation problems from those with only one or no problem. More than 1600 youths from all regions of Quebec participated in the study. These youths were around 15,7 years old when they completed an interview aiming at determining the possible presence of abusive use of psychotropic drugs, behavioral problems and feelings of depression. Their behavioral and sociofamilial characteristics had been previously evaluated (between the ages of 6 and 12) with questionnaires answered by parents and teachers. Results reveal that almost 10 % of youths experience two or three adaptation problems. These youths distinguish themselves from those with only one problem on various personal and sociofamilial dimensions in the course of childhood. Those with one problem represent a little more than 25 % of the sample. They also distinguish themselves from the group of youth with no problem on several variables. However, the group of youths with a problem of substance abuse only, is an exception. The discussion underlines the importance of knowing if there is simultaneous presence of several problems and proposes to intervene in a preventive fashion with youths who risk experiencing many problems.
 ...
PMID:[Psychoactive substance abuse, behavioral disorder and depression during adolescence.]. 1825 8

Mental or cognitive brain functions, and the effect on them of abnormal psychiatric diseases, are difficult to approach through molecular biological techniques due to the lack of appropriate assay systems with objective measures. We therefore study laws of behavioral organization, specifically how resting and active periods are interwoven throughout daily life, using objective criteria, and first discover that identical laws hold both for healthy humans subject to the full complexity of daily life, and wild-type mice subject to maximum environmental constraints. We find that active period durations with physical activity counts successively above a predefined threshold, when rescaled with individual means, follow a universal stretched exponential (gamma-type) cumulative distribution, while resting period durations below the threshold obey a universal power-law cumulative distribution with identical parameter values for both of the mammalian species. Further, by analyzing the behavioral organization of mice with a circadian clock gene (Period2) eliminated, and humans suffering from major depressive disorders, we find significantly lower parameter values (power-law scaling exponents) for the resting period durations in both these cases. Such a universality and breakdown of the behavioral organization of mice and humans, revealed through objective measures, is expected to facilitate the understanding of the molecular basis of the pathophysiology of neurobehavioral diseases, including depression, and lay the foundations for formulating a range of neuropsychiatric behavioral disorder models.
 ...
PMID:Of mice and men--universality and breakdown of behavioral organization. 1844 12

This study proposed to estimate the prevalence of behavioral disorders and associated factors in adolescents (11-15 years), using a cross-sectional design (n = 1,145). Subjects answered a self-administered questionnaire. Behavioral disorder was assessed with the Mini International Neuropsychiatric Interview (MINI). The study analyzed disorders in relation to gender, age, socioeconomic status, schooling, failure in school, religion, smoking, sedentary lifestyle, alcohol consumption, drug use, depression, and bullying (as victim). Ordinal regression was used for the statistical analysis, with a hierarchical model for the outcome. An estimated 29.2% of the sample presented behavioral disorders. In the multivariate analysis, the odds ratio for a male adolescent to present one additional point on the behavioral disorder scale was 2.04 (95%CI: 1.53-2.71). Alcohol consumption, drug use, and suffering bullying were associated with higher scores on the behavioral disorder scale. The findings also showed that the factors associated with behavioral disorder showed a strong interrelationship between health behaviors in adolescence.
 ...
PMID:[Prevalence and factors associated with behavioral disorders in adolescents: a population-based study]. 1881 77

Mucopolysaccharidosis IIIA (MPS IIIA) is a lysosomal storage disorder characterized by progressive mental deterioration and severe behavioral problems. We conducted an open-label, crossover study of the efficacy and safety of Risperidone on behavioral disorder in children with MPS IIIA. A total of 12 patients (5.5+/-2.2 years) with enzymatic diagnosis of MPS IIIA were randomly assigned to receive Risperidone (0.125-2mg/d) for 6 months. The hyperactivity and disruptive behavior level of children before and after treatment was evaluated regarding the scores from Turgay DSM IV Based Child and Adolescent Behavior Disorders Screening and Rating Scale (T-DSM-IV-S). Clinic Global Impression Scale - Severity (CGIS-S) was used for all cases for determining the psychiatric disorder severity. The anxiety and depression levels of mothers before and after treatment were evaluated using Hamilton Anxiety Scale (HAM-A) and Beck Depression Inventory (BDI). The adverse effects were evaluated by monitoring weight, serum prolactin, glucose and lipid levels. The response to the treatment was measured by decrease in values of CGI-S (from 6+/-1.12 to 2.91+/-0.66, p=0.001). According to T-DSM-IV-S scores the best improvement was observed in hyperactivity scores (16.25+/-8.57/11.58+/-7.26, p=0.001), followed by opposition/defiance (6.66+/-5.92/5.08+/-4.88, p=0.032), and conduct disorder scores (1.00+/-1.85/0.41+/-.99, p=0.67). No clinically relevant elevations in weight and serum prolactin, glucose or lipid levels have been documented (p>0.05). There was a significant decrease in anxiety and depression scores of mothers (HAM-A: 20.33+/-8.28/17.91+/-6.89, BDI: 23.58+/-7.14/20.5+/-5.93, p<0.001). To our knowledge, research on the pharmacological treatment of MPS IIIA with Risperidone has not been reported. According to our data, Risperidone appeared to be safe and effective in MPS IIIA patients.
 ...
PMID:Clinical overview of children with mucopolysaccharidosis type III A and effect of Risperidone treatment on children and their mothers psychological status. 1921 29

The proteinopathy sporadic Parkinson's disease (sPD) is the second most frequent degenerative disorder of the human nervous system after Alzheimer's disease. The alpha-synuclein inclusion body pathology (Lewy pathology) associated with sPD is distributed throughout the central, peripheral, and enteric nervous systems. The resulting nonrandom neuronal dysfunction and, in some regions, neuronal loss is reflected in a topographic distribution pattern of the Lewy pathology that, in the brain, can be staged. Except for olfactory structures and spinal cord constituents of the pain system, sensory components of the nervous system remain uninvolved or virtually intact. The most disease-related damage revolves around motor areas--particularly around superordinate centers of the limbic and visceromotor systems as well as portions of the somatomotor system. Vulnerable regions are interconnected anatomically and susceptible nerve cell types are not neurotransmitter-dependent. Not all clinical symptoms emerging in the course of sPD can be explained by a lack of dopamine in the nigrostriatal system. These include autonomic dysfunction, pain, hyposmia or anosmia, excessive daytime sleepiness, rapid eye movement (REM) sleep behavioral disorder, depression, anxiety, cognitive decline, and dementia. Against the background of the normal morphology and anatomy, the authors analyze the pathoanatomy of sPD in the nervous system at various neuropathological stages and summarize the potential functional consequences of the lesions.
 ...
PMID:Neuroanatomy and pathology of sporadic Parkinson's disease. 1923 May 52

The motor symptoms of Parkinson's disease (PD), bradykinesia, muscular rigidity, and tremor depend upon degeneration of the dopaminergic neurons in the substantia nigra pars compacta. Recent neuropathological studies show that the Lewy bodies, the intraneuronal landmark of PD, accumulate in several neuronal cell types in the brain. An ascending gradient of pathological involvement, from the medulla oblongata to neocortical areas has been reported. Thus the original view of PD as a disease characterized by selective damage of the dopaminergic neurons in the mesencephalon should be updated into the concept of a severe multisystemic neurodegenerative disorder. Additionally, the neuropathological alterations outside the substantia nigra are soundly correlated with the non-motor symptoms of PD. As a result of these findings, interest is growing in the identification of prodromal non-motor symptoms of PD. Indeed, data from the literature suggest that autonomic disturbances, olfactory dysfunctions, depression and sleep disorders (in particular REM-sleep behavior disorder) may represent prodromal non-motor symptoms of PD. Several tests are available to detect most of these symptoms. Thus, the identification of prodromal non-motor symptoms may contribute to the precocious diagnosis of PD, and might be useful in the future to test the efficacy of neuroprotective agents.
 ...
PMID:Prodromal non-motor symptoms of Parkinson's disease. 1930 May 44

In depression research, animal models are essential for better understanding of biological mechanisms, development of new agents, and showing evidence on various theories. Given the emotional feature of the disorder, people have debated, even revolted, on applying animal models to human studies. However, this logic is counter-arguable by noting the commonality of biological changes (e.g., behavioral disorder, environment maladjustment, and stress vulnerability) between human and experimental animals; moreover, genetic studies suggest further similarities. However, current animal models are insufficient to express the full dimension of mood disorders. The model concepts are often in a narrow context of antidepressant responses. The models consider stress models as equivalents of depression models. This hypothesis, however, has limitations in differentiating anxiety- and stress-related models from depression models. The models tend to focus on the depressive, but not manic, state; it is thereby a challenge to replicate depressive and manic phases in animals. The models do not have a standpoint of depressive disorder from cognitive aspects, and are unable to replicate mood disorder subtypes, such as atypical depression, dysthymia, bipolar disorder, and seasonal affective disorder. From a clinical perspective, models of treatment-resistant depression would eventually be of large benefit to enhance treatment outcomes in clinical settings.
 ...
PMID:[What clinicians expect from animal models of depression]. 1956 39

It is proposed that alpha-synucleinopathy initially affects the medulla oblongata and then progresses to more rostral brain areas ("Braak hypothesis"). According to this hypothesis, substantia nigra is affected in the later stages of PD. Another region affected in the earlier stages was reported to be olfactory bulb, although the following processes were not described in detail. On the other hand, several lines of evidence suggest that non-motor symptoms including constipation, depression, REM-sleep behavior disorder (RBD) and hyposmia may be prodromal symptoms in PD. The pathological staging postulated by the Braak hypothesis is in good agreement with the fact that these non-motor symptoms precede motor symptoms in PD, because affected brain areas in the early stages, such as dorsal vagal nucleus, locus ceruleus and olfactory bulb, are related to these non-motor features. Recently, it was reported that although half of brains corresponded to the Braak hypothesis, there were a high proportion of cases which did not fit the Braak's staging system and majority of the latter demonstrated amygdale-predominant alpha-synucleinopathy. It was also demonstrated that the Lewy pathology in olfactory bulb was closely related to the presence of alpha-synuclein pathology in amygdala. The amygdala is one of the main systems in odor perception and in PD, cortical neurons in corticomedial complex of amygdale, which have major olfactory connections, are selectively affected even in the early stages of the disease. We recently obtained the data suggesting that metabolic changes in the amygdala were associated with low scores in odor identification test. These data suggest that not only the olfactory bulb, but also the amygdala is also responsible for hyposmia in PD and that there may be another pathological process, which starts from the olfactory bulb and involves the amygdala.
 ...
PMID:[Pathophysiological process underlying Parkinson's disease: motor & non-motor symptoms]. 2003 Feb 39


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