Publications by authors named "Marija M Petrinovic"

Article Synopsis
  • Studies show that the uncinate fasciculus (UF), a brain structure connecting certain areas related to emotions and decision-making, has abnormal microstructural integrity in children with conduct problems (CP) and callous-unemotional traits (CU).
  • A parenting intervention over 14 weeks was tested to see if it could change these abnormalities, utilizing diffusion tensor imaging to measure changes in the UF's microstructure among 67 boys with CP and 43 typically developing boys.
  • Results indicated that after the intervention, boys with CP showed significant improvements in microstructural integrity, particularly those whose CU traits improved, suggesting that these brain abnormalities may be reversible with proper intervention.
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The brain is the central and most complex organ in the nervous system, comprising billions of neurons that constantly communicate through trillions of connections called synapses. Despite being formed mainly during prenatal and early postnatal development, synapses are continually refined and eliminated throughout life via complicated and hitherto incompletely understood mechanisms. Failure to correctly regulate the numbers and distribution of synapses has been associated with many neurological and psychiatric disorders, including autism, epilepsy, Alzheimer's disease, and schizophrenia.

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Background: Obstructive sleep apnea (OSA) is a chronic, highly prevalent, multi-system and sleep disorder, which may contribute to cognitive impairment and a variety of structural and neurophysiologic changes. The focus on OSA is warranted given its recognized links with major psychiatric and neurologic disorders, including Alzheimer's disease. Some preliminary studies suggest a dual effect of the inflammatory response in OSA.

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Autism spectrum disorder (ASD) affects over 1:100 of the population and costs the UK more than £32bn and the USA more than $175bn (£104bn) annually. Its core symptoms are social and communication difficulties, repetitive behaviours and sensory hyper- or hypo-sensitivities. A highly diverse phenotypic presentation likely reflects its etiological heterogeneity and makes finding treatment targets for ASD challenging.

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Individuals of many species rely on odors to communicate, find breeding partners, locate resources and sense dangers. In vertebrates, odorants are detected by chemosensory receptors of the olfactory system. One class of these receptors, the trace amine-associated receptors (TAARs), was recently suggested to mediate male sexual interest and mate choice.

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Autism spectrum disorder (ASD) is a pervasive neurodevelopmental syndrome with a high human and economic burden. The pathophysiology of ASD is largely unclear, thus hampering development of pharmacological treatments for the core symptoms of the disorder. Abnormalities in glutamate and GABA signaling have been hypothesized to underlie ASD symptoms, and may form a therapeutic target, but it is not known whether these abnormalities are recapitulated in humans with ASD, as well as in rodent models of the disorder.

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Empathy is a cornerstone of social behavior, impairments of which are characteristic of neuropsychiatric disorders such as autism and psychopathy. According to the "shared representations" theory, empathy relies on neural processes similar to those underpinning the first-hand experience of a given emotion. A recent study by Mischkowski, Crocker, and Way ( 11: 1345-1353, 2016) provides novel insights into neurobiological underpinnings of empathy by demonstrating that acetaminophen, a widely used painkiller, reduces empathy for other's physical and social pain.

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Functional magnetic resonance imaging (fMRI) has revolutionized neuroscience by opening a unique window that allows neurocircuitry function and pathological alterations to be probed non-invasively across brain disorders. Here we report a novel sustainable anesthesia procedure for small animal neuroimaging that overcomes shortcomings of anesthetics commonly used in rodent fMRI. The significantly improved preservation of cerebrovascular dynamics enhances sensitivity to neural activity changes for which it serves as a proxy in fMRI readouts.

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Excitation/inhibition imbalance is implicated in symptoms of neuropsychiatric disorders. We discuss a study by Liang et al. (Mol Psychiatry 20: 850-859, 2015) demonstrating that the conditional knockout of neuroligin-2, a postsynaptic adhesion protein, in the prefrontal cortex of adult mice results in alterations in inhibitory synaptic properties.

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Adult central nervous system axons show restricted growth and regeneration properties after injury. One of the underlying mechanisms is the activation of the Nogo-A/Nogo receptor (NgR1) signaling pathway. Nogo-A knockout (KO) mice show enhanced regenerative growth in vivo, even though it is less pronounced than after acute antibody-mediated neutralization of Nogo-A.

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Rationale: Autism spectrum disorder(s) (ASDs) is a neurodevelopmental disorder characterized by stereotyped behaviours and impairments in communication and social interactions. This heterogeneity has been a major obstacle in uncovering the aetiology and biomarkers of ASDs. Rodent models with genetic modifications or environmental insults have been created to study particular endophenotypes and bridge the gap between genetics and behavioural phenotypes.

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Neuronal signal integration as well as synaptic transmission and plasticity highly depend on the morphology of dendrites and their spines. Nogo-A is a membrane protein enriched in the adult central nervous system (CNS) myelin, where it restricts the capacity of axons to grow and regenerate after injury. Nogo-A is also expressed by certain neurons, in particular during development, but its physiological function in this cell type is less well understood.

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Wiring of the nervous system is a multi-step process involving complex interactions of the growing fibre with its tissue environment and with neighbouring fibres. Nogo-A is a membrane protein enriched in the adult central nervous system (CNS) myelin, where it restricts the capacity of axons to grow and regenerate after injury. During development, Nogo-A is also expressed by neurons but its function in this cell type is poorly known.

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