Tuberous Sclerosis Complex
Dongyou Liu in Handbook of Tumor Syndromes, 2020
Cortical tubers are regions of cortical dysplasia that likely result from aberrant neuronal migration during corticogenesis and are observed in ∼90% of TSC patients [2,28]. Dysplastic neurons have disrupted radial orientation in the cortex and abnormal dendritic arborization, showing γ-aminobutyric acid (GABA)-transporter defect and low GABAergic inhibition [1,78]. Tubers are static lesions with variable size and can be multiple in the same individual [77]. They are directly related to the more prevalent neurologic manifestations of TSC, including epilepsy, cognitive impairment, challenging behavioral problems, and autism [13]. These symptoms are highly variable in age at onset and can be detected by fetal MRI or pathological findings as early as 26 weeks of gestation [42]. Cerebral white matter radial migration lines arise from a similar pathologic process as cortical tubers and can be observed in 20%–30% of patients [77]. It is not unusual to find tubers and white matter migrational abnormalities together [2].
Thymus and Neuro-Endocrine-Immune Regulation of Homeostasis
Marek P. Dabrowski, Barbara K. Dabrowska-Bernstein in Immunoregulatory Role of Thymus, 2019
On the grounds of these data, Hall et al. considered the possibility of a central site of action of thymosin which could result in an increased corticogenesis.154 To test the hypothesis, they first used an in vitro model of isolated adrenal fasciculata cells which normally respond to ACTH with elaboration of glucocorticoids and cAMP. In contrast to the ACTH effects, neither cAMP nor corticosterone release were increased by different regimes of incubation with thymosin fraction 5 or thymosin alpha 1. The thymosins were also unable to potentiate the stimulatory effects of ACTH. In consequence, the authors assumed that the corticogenic effects of thymic hormones could hardly be due to direct stimulation of the adrenal cortex. As the other possible site of thymosin action could be the pituitary cells which produce ACTH, the minced pituitary tissue from adult rats was superfused with thymosin fraction 5 in the next experiment. The results were negative again, as, in contrast to the significant release of ACTH into the medium triggered by corticotropin releasing factor (CRF), the addition of thymosin fraction 5 was without any effect. The pituitary cells were still viable after thymosin treatment as indicated by the preserved ability to release ACTH in response to the subsequent stimulation with CRF. The results, then, were consistently negative for the adrenal cortex and for anterior pituitary as possible sites of thymosin action.
Conclusion
Ivanka V. Asenova in Brain Lateralization and Developmental Disorders, 2018
I consider the DI model much more promising and I believe that future empirical studies of developmental disorders’ subtypes inspired by the DI theory could find key answers concerning the etiopathogenetic mechanisms of different forms of neurodevelopmental pathology, and in particular, the role of the atypical asymmetrical development of the cerebral cortex in their origin.
Stigmasterol promotes neuronal migration via reelin signaling in neurosphere migration assays
Published in Nutritional Neuroscience, 2020
During development of the cerebral cortex, neurons are generated at the subventricular zone and subsequently migrate to specified cortical regions.32 Disorders of neuronal migration result in periventricular heterotopia (abnormal nodules of neurons located along the ventricular wall), lissencephaly (smooth brain), subcortical band heterotopia (heterotopic neurons located midway between the brain surface and lateral ventricles), and cobblestone lissencephaly.32,33 In a previous study, we found by transcriptome analysis that ST induces the expressions of migration-related genes, such as Axl, Bbs4, Cntn2, Dcx, Erbb4, Gja1, Ntrk2, Pcm1, Ptprz1 and Reln.9 In the present study, we first confirmed this transcriptome result in a neurosphere migration assay using cultured E14 primary cortical neurons, which aggregate to form neurospheres.16 During migration, centrosomes lie between the nucleus and the leading edge of neurons, and this phenomenon is referred to as ‘centrosome reorientation’.34 This anterior nuclear-centrosome (NC) axis orientation (aka ‘centrosome reorientation’) is observed in many cell types migrating on two dimensional (2D) surfaces,34 and in neurons migrating in 3D substrata.35 As assessed by centrosome reorientation, ST significantly increased the percentage of migratory cells from 32% to average 47% of total cells in the neurospheres. In addition to the percentage increase of the migrating neurons, ST also increased the distance they migrated. These results indicate ST induces neuronal migration.
Secretagogin may not be a new neuroendocrine biomarker in schizophrenia while levels may reflect clinical severity
Published in Psychiatry and Clinical Psychopharmacology, 2019
Gamze Erzin, Canan Topçuoğlu, Şenol Bayram, Hasan Karadağ, Güven Ozkaya, Turan Turhan, Erol Göka
SCGN might be a biomarker for endocrine tumors, stroke, and psychiatric conditions. Secretagogin has been hypothetically suggested to have a neuroprotective role in neurodegenerative diseases [7]. Raju et al. was examined the effects of SCGN expression on GABAergic neuron function and form [8]. In schizophrenia, specific subpopulations of GABA neurons have been reported to be severely affected [9–14]. SCGN expression has cell-intrinsic effects on neuronal morphology. Beyond these effects, it is important to recognize that GABA signalling provides excitatory drive for immature neocortical networks. GABA signalling has been also implicated in most aspects of corticogenesis such as proliferation, migration, and synaptogenesis [15]. SCGN’s role in cellular defense against neuronal damage, makes it important to investigate in schizophrenia [3,16,17]. For all these reasons, we suggest that SCGN may be associated with psychiatric conditions, especially with schizophrenia. Therefore, in this study, we aimed to evaluate serum secretagogin levels in patients with non-diabetic schizophrenia who had antipsychotic use.
Smoking by pregnant mothers and risk of future tobacco use by offspring: a meta-analysis
Published in Journal of Substance Use, 2022
Nicotine dependence is most likely to develop during one of two periods of vulnerability – the prenatal period and adolescence(Mamun, Lawlor et al., 2006) . The adolescent period is critical to cortical development. The frontal cortex develops late in adolescence and helps refine reasoning, setting of priorities and goals, impulse control, and evaluation of long- and short-term rewards (Crews et al., 2007). Therefore, adolescents are particularly vulnerable to addiction. However, prenatal nicotine exposure also influences offspring corticogenesis. Nicotine can transverse the placental barrier, subjecting the fetus to nicotine blood concentrations that exceed those of the mother(Wickstrom, 2007).This phenomenon can result in modifications to the specific neural circuitry of the fetus. Such changes to the function and structure of the brain may lead to clinically characterized deficits, such as sudden infant death syndrome and auditory-cognitive dysfunction (Dwyer et al., 2008). In the fourth gestational week, fetuses develop nicotine acetylcholine receptors, and nicotine exposure thereafter is suggested to produce sensitization and disruption of the pathways mediated by acetylcholine as well as potential birth defects. These changes in children/fetuses or offspring can increase their susceptibility to nicotine dependence. Indeed, uteroexposure to nicotine in rats has been demonstrated to affect the development of the dopaminergic and central serotonergic systems of offspring. Therefore, fetuses exposed to nicotine may experience alterations in the pathways associated with drug rewards.
Related Knowledge Centers
- Axon
- Cerebral Cortex
- Myelin
- Brain
- Development of The Nervous System
- Development of The Nervous System In Humans
- Neuron
- Ventricular Zone
- Grey Matter
- White Matter