Abstract:
:Prenatal stress has been associated with increased vulnerability to psychiatric disturbances including schizophrenia, depression, attention-deficit hyperactivity disorder and autism. Elevated maternal circulating stress hormones alter development of neural circuits in the fetal brain and cause long-term changes in behaviour. The aim of the present study was to investigate whether mild prenatal stress increases the vulnerability of dopamine neurons in adulthood. A low dose of 6-hydroxydopamine (6-OHDA, 5 microg/4 microl saline) was unilaterally infused into the medial forebrain bundle of nerve fibres in the rat brain in order to create a partial lesion of dopamine neurons which was sufficient to cause subtle behavioural deficits associated with early onset of Parkinson's disease without complete destruction of dopamine neurons. Voluntary exercise appeared to have a neuroprotective effect resulting in an improvement in motor control and decreased asymmetry in the use of left and right forelimbs to explore a novel environment as well as decreased asymmetry of tyrosine hydroxylase-positive cells in the substantia nigra pars compacta and decreased dopamine cell loss in 6-OHDA-lesioned rats. Prenatal stress appeared to enhance the toxic effect of 6-OHDA possibly by reducing the compensatory adaptations to exercise.
journal_name
Metab Brain Disjournal_title
Metabolic brain diseaseauthors
Mabandla MV,Kellaway LA,Daniels WM,Russell VAdoi
10.1007/s11011-009-9161-6subject
Has Abstractpub_date
2009-12-01 00:00:00pages
525-39issue
4eissn
0885-7490issn
1573-7365journal_volume
24pub_type
杂志文章abstract::Pipecolic acid (PA) levels are increased in severe metabolic disorders of the central nervous system such as Zellweger syndrome, infantile Refsum disease, neonatal adrenoleukodystrophy and hyperlysinemia. The affected individuals present progressive neurological dysfunction, hypotonia and growth retardation. The mecha...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-013-9466-3
更新日期:2014-03-01 00:00:00
abstract::Lactic acid accumulation has been implicated in the evolution of brain damage after ischemia. Since compartmentation of lactate may play a role in acid-base balance, lactate release from gerbil hippocampal slices was examined during a number of metabolic stresses including elevated [K+]e, ischemia, anoxia, and aglycem...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF00999841
更新日期:1990-09-01 00:00:00
abstract::Several studies have examined neonatal diabetes, a rare disease characterized by hyperglycemia and low insulin levels that is usually diagnosed in the first 6 month of life. Recently, the effects of diabetes on the brain have received considerable attention. In addition, hyperglycemia may perturb brain function and mi...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-017-0170-6
更新日期:2018-02-01 00:00:00
abstract::Despite many clinical trials assessing the role of zinc in major depressive disorder (MDD), the conclusions still remain ambiguous. The aim of the present clinical study was to determine and comparison the zinc concentration in the blood of MDD patients (active stage or remission) and healthy volunteers (controls), as...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-016-9888-9
更新日期:2017-02-01 00:00:00
abstract::D-glycerate 2 kinase (DGK) is an enzyme that mediates the conversion of D-glycerate, an intermediate metabolite of serine and fructose metabolism, to 2-phosphoglycerate. Deficiency of DGK leads to accumulation of D-glycerate in various tissues and its massive excretion in urine. D-glyceric aciduria (DGA) is an autosom...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-019-0384-x
更新日期:2019-04-01 00:00:00
abstract::Hepatic encephalopathy (HE) is an important cause of morbidity and mortality in patients with severe liver disease. Although the molecular basis for the neurological disorder in HE remains elusive, elevated ammonia and its chief metabolite glutamine are believed to be important factors responsible for altered cerebral...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1023/a:1011666612822
更新日期:2001-06-01 00:00:00
abstract::To characterize an Egyptian patient with glutaric acidemia type I (GA I) and to identify the causative mutation(s) that may be responsible for the disease phenotype. MRI was performed on the patient using the 1.5 T magnet, biochemical analysis was carried out using gas chromatography/mass spectrometry on the patient's...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-016-9879-x
更新日期:2017-02-01 00:00:00
abstract::D-Galactose (D-gal) chronic administration via intraperitoneal and subcutaneous routes has been used as a model of aging and Alzheimer disease in rodents. Intraperitoneal and subcutaneous administration of D-gal causes memory impairments, a reduction in the neurogenesis of adult mice, an increase in the levels of the ...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-017-9972-9
更新日期:2017-06-01 00:00:00
abstract::To assess whether EGb761 could protect elderly diabetic mice with cognitive disorders and explore the role of beclin-1-mediated autophagy in these protective effects. Two-month-old male db/db-/- mice and wild-type C57/BL6 mice were randomly divided into six groups: db/db-/- control, db/db-/- 50 mg, db/db-/- 100 mg, wi...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-018-0295-2
更新日期:2018-12-01 00:00:00
abstract::Tyrosinemia type II is an inborn error of metabolism caused by a deficiency in hepatic cytosolic aminotransferase. Affected patients usually present a variable degree of mental retardation, which may be related to the level of plasma tyrosine. In the present study we evaluated effect of chronic administration of L-tyr...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-014-9615-3
更新日期:2015-02-01 00:00:00
abstract::Brain glucose uptake is usually reduced in type 2 diabetes owing to downregulation of brain glucose transporters. The ability of Vernonia amygdalina to stimulate glucose uptake as well as ameliorate glucose-induced oxidative stress and proinflammation were investigated in rat brain. Hot infusion of V. amygdalina leave...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-018-0363-7
更新日期:2019-06-01 00:00:00
abstract::The free radical scavenging abilities of the structurally related steroids beta-sitosterol, beta-sitosterol glucoside (plant sterols and sterolins), cholesterol, and dehydroepiandrosterone sulphate (DHEAS) were compared with melatonin (an efficient free radical scavenger) in an in vitro system which measures lipid per...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1023/a:1011167023695
更新日期:2000-12-01 00:00:00
abstract::Following axonal interruption, structural, metabolic and physiological parameters change in motorneurons. Also, glial cells are involved in this process. Microglia proliferate and express new proteins such as vimentin or MHC antigens. Astrocytes show hypertrophy, increased GFAP synthesis, and formation of lamellae. Bo...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/BF00999498
更新日期:1989-03-01 00:00:00
abstract::The developing facial neurons of a series of hamsters ranging in age from the 14-day fetus to the 9 day postnatal were axotomized. Postoperative times were graded for each age so that the retrograde response could be observed before any significant amount of cell degeneration or death occurred. The incorporation of tr...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF00996894
更新日期:1993-06-01 00:00:00
abstract::Increased benzodiazepine (BZ) receptor density has been reported in brains of rabbits with hepatic encephalopathy (HE) due to galactosamine (GalN)-induced fulminant hepatic failure (FHF). These data were generated using detergent-Triton X-100-treated neural membranes. While performing further studies it was noted that...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF01000296
更新日期:1989-09-01 00:00:00
abstract::Hyperphenylalaninemia (HPA) leads to increased oxidative stress in patients with phenylketonuria (PKU) and in animal models of PKU. Early diagnosis and immediate adherence to a phenylalanine-restricted diet prevents HPA and, consequently, severe brain damage. However, treated adolescent and adult PKU patients have dif...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-013-9414-2
更新日期:2013-12-01 00:00:00
abstract::Chronic exposure to stress amplifies locomotor deficits and exacerbates dopamine neuron loss in an animal model for Parkinson's disease. The release of neurotrophic factors such as glial cell-line derived neurotrophic factor (GDNF) and neurotrophin-3 (NT-3) following neuronal injury attenuates exacerbated degeneration...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-017-9988-1
更新日期:2017-08-01 00:00:00
abstract::The present study analyses the potential role of MTHFR gene polymorphism, folate supplementation and dietary pattern among the mothers of NTD neonates and controls in heterogeneous populations of North India, with the special focus on their ethnic labels. Results indicated significant increased risk for neural tube de...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-011-9256-8
更新日期:2011-09-01 00:00:00
abstract::There is substantial clinical and experimental evidence that ammonia is a major factor in the pathogenesis of hepatic encephalopathy. In the article is demonstrated that in hepatocellular dysfunction, ammonia detoxification to glutamine (GLN) in skeletal muscle, brain, and likely the lungs, is activated. In addition t...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-013-9428-9
更新日期:2014-03-01 00:00:00
abstract::In view of the protective effect of brain derived neurotrophic factor (BDNF) against metabolic/excitotoxic insults in vitro, we investigated whether BDNF could limit infarct size after permanent occlusion of the middle cerebral artery in rat (MCAO). BDNF was delivered into the territory of the middle cerebral artery v...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/BF02674671
更新日期:1997-12-01 00:00:00
abstract::Chronic neuroinflammation is strongly associated with AD and altered peripheral and central levels of chemokines and cytokines have been frequently described in those with AD. Given the increasing evidence of ethnicity-related differences in AD, it was of interest to determine if those altered chemokine and cytokine l...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-019-00512-2
更新日期:2020-01-01 00:00:00
abstract::Aberrant brain functional connectivity has been considered as the important mechanism underlying minimal hepatic encephalopathy (MHE); however, little is known about the change in interhemispheric connection in MHE patients. Twenty patients with HBV-related cirrhosis and MHE and 15 healthy controls were included in th...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-014-9505-8
更新日期:2014-09-01 00:00:00
abstract::Increasing evidence indicates that excessive drug consumption is sufficient for the transition from recreational and controlled drug use to uncontrolled use and addiction. However, the underlying mechanisms are debated. Some neurobehavioral and neuroimaging evidence indicates that dorsolateral striatum (dlStr)-depende...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-019-00430-3
更新日期:2019-08-01 00:00:00
abstract::A study evaluating zinc supplementation in patients with Alzheimer's disease yielded variable zinc plasma levels in spite of positive cognitive and physiological results. In an attempt to raise and sustain plasma zinc levels, a single patient was given 15 mg zinc/day with various combinations of vitamins. A sustained ...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-006-9023-4
更新日期:2006-09-01 00:00:00
abstract::Hepatic encephalopathy can be a life-threatening complication of fulminant hepatic failure. By understanding the pathophysiology involved in the induction of this neuropsychiatric disorder, future therapeutic and/or preventive attempts could be considered. In this study, an attempt has been made in order to shed more ...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-008-9091-8
更新日期:2008-09-01 00:00:00
abstract::Hyperammonemia is necessary for development of the cerebral complications to liver disease including hepatic encephalopathy and cerebral edema but the mechanisms are unclear. Ammonia is taken up by the brain in proportion to its arterial concentration. The flux into the brain is most likely by both diffusion of NH3 an...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-014-9494-7
更新日期:2014-12-01 00:00:00
abstract::Isolated Methylmalonic acidemia/aciduria (MMA) is a group of inborn errors of metabolism disease which is caused by defect in methylmalonyl-CoA mutase (MCM) enzyme. The enzyme has a key function in the catabolism of branched chain amino acids (BCAA, isoleucine, and valine), methionine, and threonine. MCM is encoded by...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-018-0277-4
更新日期:2018-10-01 00:00:00
abstract::Hepatic encephalopathy (HE) is a neuropsychiatric syndrome which develops in patients with severe liver diseases and/or portal-systemic shunting. Minimal HE, the earliest manifestation of HE, has drawn increasing attention in the last decade. Minimal HE is associated with a series of brain functional changes, such as ...
journal_title:Metabolic brain disease
pub_type: 杂志文章,评审
doi:10.1007/s11011-014-9504-9
更新日期:2014-09-01 00:00:00
abstract::In patients with hepatic encephalopathy (HE) the blood concentration of ammonia is usually highly elevated. Ammonia readily enters brain cells from the blood, and toxic effects of ammonia on brain metabolism and neurotransmission are believed to play a key role in the pathogenesis of HE. It has, however, been a matter...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1007/s11011-008-9126-1
更新日期:2009-03-01 00:00:00
abstract::A rat model of glucose-precipitated Wernicke's encephalopathy (WE) has been developed in which glucose loading (10 g/kg, i.p.) of ataxic thiamin-deficient (TD) rats induced episodes of gross neurological dysfunction and sometimes death. The acute effects of a glucose load on the neurological state of thiamin-replete c...
journal_title:Metabolic brain disease
pub_type: 杂志文章
doi:10.1023/a:1020653312697
更新日期:1999-03-01 00:00:00