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Query: UMLS:C0036341 (
schizophrenia
)
60,220
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Schizophrenia
is a debilitating mental disorder that afflicts about 1% of the population worldwide. Despite intensive, multifaceted research, its exact etiology remains elusive. Epidemiological data shows that when pregnant mothers experienced malnutrition or famine (e.g. the Dutch
Hunger
Winter of 1994-1945 and the Chinese famine of 1959-1961), the risk of
schizophrenia
in their children increased by two fold. This fact could be considered in the context of Developmental Origins of Health and Disease (DOHaD) or fetal programming. The concept of DOHaD is well referenced in the understanding of adult metabolic diseases, but less so in the field of mental disorders. We will attempt to show how the mechanisms of DOHaD could contribute at least in part to
schizophrenia
pathogenesis. Resonating with this concept, we introduce mainly our data showing increased expression of genes for fatty acid binding proteins (FABPs) in the postmortem brains from patients with
schizophrenia
and the beneficial effect conferred by the administration of polyunsaturated fatty acids (PUFAs) during the early developmental period of rats.
...
PMID:Role of polyunsaturated fatty acids and fatty acid binding protein in the pathogenesis of schizophrenia. 2135 37
An increasing body of evidence suggests that poor nutrition at the very beginning of life - even before birth - leads to large and long term negative consequences for both mental and physical health. This paper reviews the evidence from studies on the Dutch famine, which investigated the effects of prenatal undernutrition on later health. The effects of famine appeared to depend on its timing during gestation, and the organs and tissues undergoing critical periods of development at that time. Early gestation appeared to be the most vulnerable period. People who were conceived during the famine were at increased risk of
schizophrenia
and depression, they had a more atherogenic plasma lipid profile, were more responsive to stress and had a doubled rate of coronary heart disease. Also, they performed worse on cognitive tasks which may be a sign of accelerated ageing. People exposed during any period of gestation had more type 2 diabetes. Future investigation will expand on the finding that the effects of prenatal famine exposure may reach down across generations, possibly through epigenetic mechanisms. Recent evidence suggests that similar effects of prenatal undernutrition are found in Africa, where many are undernourished.
Hunger
is a major problem worldwide with one in seven inhabitants of this planet suffering from lack of food. Adequately feeding women before and during pregnancy may be a promising strategy in preventing chronic diseases worldwide.
...
PMID:Hungry in the womb: what are the consequences? Lessons from the Dutch famine. 2180 26
Auricular acupressure is widely used in complementary and alternative medicine to reduce body weight, but little is known about the effects of auricular acupressure on body weight parameters in patients with chronic schizophrenia. The purpose of this study was to evaluate the effects of auricular acupressure on body weight parameters in patients with chronic schizophrenia. Eighty-six inpatients with
schizophrenia
were recruited from chronic wards in a psychiatric center. The participants were randomly divided into experimental (acupressure at 4 acupuncture sites:
hunger
, stomach, shenmen and endocrine) and control groups, and body weight parameters were determined weekly for 8 weeks. There was no significant difference between the experimental and control groups in mean body weight, waist circumference, or body fat percentage at the pretest or during the entire 8-week study period. Therefore, auricular acupressure did not cause body weight reduction in patients with chronic schizophrenia.
...
PMID:Effects of auricular acupressure on body weight parameters in patients with chronic schizophrenia. 2299 27
Health consequences of relative or absolute poverty constitute a definitive area of study in social medicine. As demonstrated in the extreme example of the Dutch
Hunger
Winter from 1944 to 1945, prenatal
hunger
can lead to adult
schizophrenia
and depression. A Norwegian study showed how childhood poverty resulted in a heightened risk of myocardial infarction in adulthood. In England, a study of extended impaired prenatal nutrition indicated three different types of increased cardiovascular risk at older ages. Current animal and human studies link both adverse and enriched environmental exposures to intergenerational transmission. We do not fully understand the molecular mechanisms for it; however, studies that follow up epigenetic marks within a generation combined with exploration of gametic epigenetic inheritance may help explain the prevalence of certain conditions such as cardiovascular disease,
schizophrenia
, and alcoholism, which have complex etiologies. Insights from these studies will be of great public health importance.
...
PMID:Intergenerational health responses to adverse and enriched environments. 2329 58
Up until October 2012, Kohnodai Hospital had introduced clozapine treatment for 55 cases of treatment-resistant
schizophrenia
. In all cases, previous antipsychotic medication was discontinued the day before clozapine administration began. Of the 55 cases, 45(85%)are continuing clozapine administration, and 40 cases (73%) are receiving outpatient treatment. The average dose of clozapine was 373.1 mg/day (SD : 160.5). Clozapine was administered for a month or more in 51 cases (93%). BPRS scores improved 20% or more in a month's administration of clozapine in 18 of the cases (35%). The average clozapine dose in the improvement cases was 176 mg/day. The average BPRS score had significantly decreased from the baseline at months 1, 3, 6, and 12 after the start of clozapine administration. Of the 33 cases receiving clozapine treatment for 12 months or more, BPRS improved 20% or more in 27 (82%). BPRS improved 20% or more for the first time after clozapine administration within a month in 12 cases (44%), 3 months in 8 cases (30%), 6 months in 5 cases (19%), and 12 months in 2 cases (7%). These results suggest that clozapine should be administered continuously for over 6 months at the least and 12 months if possible to evaluate the efficacy of clozapine treatment. Of the 43 cases receiving outpatient clozapine therapy, the average GAF score improved significantly from the time of ward admission to discharge (20.6 and 42.0, respectively). Clozapine had to be discontinued in 2 cases of leukopenia, 2 cases of neutropenia, 1 case of reduced left ventricular ejection due to pericardial effusion, 1 case of drug eruption, and 1 case of marked
hunger
. When introducing clozapine for treatment-resistant
schizophrenia
, it is important to administer it as a monotherapy, slowly increase the dosage to reduce side effects, and achieve a treatment effect at the minimum required dosage.
...
PMID:[Clinical experience with clozapine in 55 cases of treatment-resistant schizophrenia]. 2422 73
Nogo-A is an important neurite growth-regulatory protein in the adult and developing nervous system. Mice lacking Nogo-A, or rats with neuronal Nogo-A deficiency, exhibit behavioral abnormalities such as impaired short-term memory, decreased pre-pulse inhibition, and behavioral inflexibility. In the current study, we extended the behavioral profile of the Nogo-A deficient rat line with respect to reward sensitivity and motivation, and determined the concentrations of the monoamines dopamine and serotonin in the prefrontal cortex (PFC), dorsal striatum (dSTR), and nucleus accumbens (NAcc). Using a limited access consumption task, we found similar intake of a sweet condensed milk solution following ad libitum or restricted feeding in wild-type and Nogo-A deficient rats, indicating normal reward sensitivity and translation of
hunger
into feeding behavior. When tested for motivation in a spontaneous progressive ratio task, Nogo-A deficient rats exhibited lower break points and tended to have lower "highest completed ratios." Further, under extinction conditions responding ceased substantially earlier in these rats. Finally, in the PFC we found increased tissue levels of serotonin, while dopamine was unaltered. Dopamine and serotonin levels were also unaltered in the dSTR and the NAcc. In summary, these results suggest a role for Nogo-A regulated processes in motivated behavior and related neurochemistry. The behavioral pattern observed resembles aspects of the negative symptomatology of
schizophrenia
.
...
PMID:Reduced expression of nogo-a leads to motivational deficits in rats. 2447 57
A compulsive phenotype characterizes several neuropsychiatric illnesses - including but not limited to -
schizophrenia
and obsessive compulsive disorder. Because of its perceived etiological heterogeneity, it is challenging to disentangle the specific neurophysiology that precipitates compulsive behaving. Using polydipsia (or non-regulatory water drinking), we describe candidate neural substrates of compulsivity. We further postulate that aberrant neuroplasticity within cortically projecting structures [i.e., the bed nucleus of the stria terminalis (BNST)] and circuits that encode homeostatic emotions (thirst,
hunger
, satiety, etc.) underlie compulsive drinking. By transducing an inaccurate signal that fails to represent true homeostatic state, cortical structures cannot select appropriate and adaptive actions. Additionally, augmented dopamine (DA) reactivity in striatal projections to and from the frontal cortex contribute to aberrant homeostatic signal propagation that ultimately biases cortex-dependent behavioral selection. Responding becomes rigid and corresponds with both erroneous, inflexible encoding in both bottom-up structures and in top-down pathways. How aberrant neuroplasticity in circuits that encode homeostatic emotion result in the genesis and maintenance of compulsive behaviors needs further investigation.
...
PMID:The Bed Nucleus of the Stria Terminalis, Homeostatic Satiety, and Compulsions: What Can We Learn From Polydipsia? 3141 76
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