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Improved Management of Autism Spectrum Disorder (ASD) by Micronutrients
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
In autopsied cerebellar cortex samples of ASD patients, the expression of 9 miRs were altered.43 These miRs target mRNA of neurexin and SHANK3. Abnormalities in these proteins are linked with ASD. In the autopsied brain samples of ASD patients, the expression of miR-142-5p, miR-142-3p, miR-451a, miR-144-3p, and miR-21-5p were upregulated. In addition, the promoter region of the miR-142 was hypomethylated, suggesting that epigenetics is an important factor in dysregulation of microRNA. These miRs target mRNAs destined to be translated into proteins involved in synaptic function. Further analysis revealed that miR-451a and miR-21-5p target mRNA for oxytocin receptor (OXTR). Overexpression of miR-21-5p reduces the levels of OXTR by binding with 3′-UTR OXTR mRNA.44 In autopsied brain samples of ASD patients, the expression of miR-4753-5p and miR-1 in the superior temporal sulcus (STS), and miR-664-3p, miR-4709-3p, miR-4742-3p, and miR-297 in the primary auditory cortex (PAC) was differently expressed compared with controls.45 MicroRNAs in each brain region targeted mRNAs that are involved in making cell cycle protein and canonical signaling pathways, including P13-Akt that are implicated in ASD. MicroRNAs impaired immune pathways only in the STS. Small non-coding RNAs (snoRNAs) and pre-miR were also differentially expressed in ASD patients compare with control subjects.
Principles of Treatment for Arthropod Bites, Stings, and Other Exposure
Published in Gail Miriam Moraru, Jerome Goddard, The Goddard Guide to Arthropods of Medical Importance, Seventh Edition, 2019
Gail Miriam Moraru, Jerome Goddard
Widow spiders and some scorpions produce ill effects in humans by neurotoxic venoms. The primary toxin in widow spider (Latrodectus spp.) venom is α-latrotoxin which binds to specific presynaptic receptors (neurexin 1a and CIRL), precipitating neurotransmitter release, particularly norepinephrine and acetylcholine.13 This leads to sweating, piloerection, muscular spasm, weakness, tremor, and sometimes paralysis, stupor, and convulsions. This type of venom may not produce obvious skin lesions but will primarily produce these systemic reactions.
Genetic influences on antisocial behaviour, problem substance use and schizophrenia: evidence from quantitative genetic and molecular genetic studies
Published in John C. Gunn, Pamela J. Taylor, Forensic Psychiatry, 2014
Pamela J Taylor, Marianne BM van den Bree, Nigel Williams, Terrie E Moffitt
More recently, the application of techniques that allow the detection of CNVs at a higher resolution has revealed further evidence that some rare CNVs increase risk of developing schizophrenia. First, two independent studies identified deletions intersecting the neurexin 1 gene (NRXN1), located at chromosome 2p16.3, in schizophrenia cases (Walsh et al., 2008; Kirov et al., 2008). These findings were particularly intriguing as the NRXN1 protein plays a vital role in GABAergic and glutamatergic synaptic differentiation (Craig and Kang, 2007), making it an excellent candidate for schizophrenia. These were followed by the simultaneous publication of two more studies, both of which identified CNVs at 22q11.21, 1q21.1 and 15q13.3 to be significantly associated with schizophrenia (Stefansson et al., 2008; the International Schizophrenia Consortium, 2000). In addition, one study identified significant enrichment of CNVs at 15q11.22 (Stefansson et al., 2008). All of these regions harbour a large number of contiguous genes; however, while not reported as part of the main findings, both of these studies also identified a predominance of rare deletions at the NRXN1 locus in people with schizophrenia (Kirov et al., 2009). In addition, by carefully collating several large datasets, two studies have now demonstrated that people with schizophrenia carry a highly significant excess of CNVs at both chromosomes 16p13 (p = 0.0001) and 16p11 (p = 4.8×10-7) (Ingason et al., 2011; McCarthy et al., 2009).
The effect of vitamin B12 on synaptic plasticity of hippocampus in Alzheimer’s disease model rats
Published in International Journal of Neuroscience, 2023
Jahanshahi Mehrdad, Elyasi Leila, Nikmahzar Emsehgol
Another important finding of our study was the effect of vitamin B12 on cell–adhesion molecules. The cell–adhesion molecules, localized at synapses, are vital for synapse specification and integrity [27]. They also show signaling properties by interacting with their partners, organizing the neurotransmission machinery on either directions of the synapses [28]. Neurexins are important cell–adhesion molecules in synapses of the nervous system [29] and PSD–95 is the main protein of postsynaptic density that mediates NMDA receptors clustering within synapses. Both, neurexins and PSD–95, can regulate the balance between excitatory and inhibitory synapses [30]. Therefore, we measured PSD–95, neurexin1, and neuroligin for assessment of the synaptic integrity of hippocampus in the experimental groups and the results showed that concentrations of PSD–95 and neurexin1 proteins were reduced in hippocampus. Abnormalities in the amounts of synaptic proteins in scopolamine–induced AD in the rats, observed in the present study, are possibly because of the progress in the pathological conditions associated with AD and vitamin B12 could attenuate these effects, possibly by prevention of the synaptic degradation leading to neuronal death, as vitamin B12 is a determinant factor linked to neurogenesis [31]. Yet, the precise mechanisms and neurogenesis induced by vitamin B12, the potential functional associations between the neuroprotection of vitamin B12 and interactions between synaptic proteins, and the right signaling routes of vitamin B12 in CNS are unknown.
Nitric oxide pathway as a plausible therapeutic target in autism spectrum disorders
Published in Expert Opinion on Therapeutic Targets, 2022
Rishab Mehta, Anurag Kuhad, Ranjana Bhandari
The aforementioned genetic alterations alter functions, morphology, and biological pathways of the brain leading to the pathogenesis of autistic syndromes. Many of these genetic changes tend to alter synaptic transmission as well as synaptogenesis [22]. These genetic changes also tend to produce behavioral alterations such as repetitive and restrictive behavior, stereotypy, social interaction, and communication deficits. In syndromic autism, there is a change in neocortical inhibitory and excitatory balance along with long-term change in synaptic plasticity [6,15]. There are many well-described autism susceptible genes such as neurolignins, neurexins including CNTNAP 2 and human serotonin transporter along with human oxytocin receptor genes and many others [23]. MECP2 gene mutations that cause Rett syndrome result in the disruption of GABAergic neurons [24]. The disruption of GABAergic interneurons as well as changes in neuronal cytoskeleton along with dendritic changes are known to be associated with etiology of autistic disorders. The assumption of excitation-inhibition imbalance in ASDs is supported by the fact that at least 30% of the ASD patients also have epilepsy [25].
Synaptic remodeling, lessons from C. elegans
Published in Journal of Neurogenetics, 2020
Andrea Cuentas-Condori, David M. Miller, 3rd
Recent studies have confirmed that dendritic spines in C. elegans DD and VD GABAergic motor neurons display key hallmarks of mammalian spines as they (1) are structurally defined by a dynamic actin cytoskeleton, (2) localize postsynaptic proteins in apposition to excitatory presynaptic terminals (Figure 7(B,C)), (3) localize ER and ribosomes, (4) display Ca++ transients evoked by presynaptic activity and, (5) respond to activity-dependent signals that modulate spine density (Cuentas-Condori et al., 2019; Philbrook et al., 2018). Interestingly, postsynaptic spine formation and maintenance requires the trans-synaptic adhesion protein Neurexin/NRX-1, which functions in presynaptic cholinergic motor neurons. Surprisingly, this Neurexin/NRX-1-dependent effect does not require the canonical trans-synaptic interacting partner, the membrane protein neuroligin/NLG-1 and thus likely interacts with an alternative component that is currently unknown (Philbrook et al., 2018). The dramatic emergence of dendritic spines in remodeling DD neurons offers a unique opportunity to exploit the power of C. elegans genetics and live cell imaging to define evolutionarily ancient but shared mechanisms that drive spine morphogenesis.