REMOVED: Identification of shared and distinct electrophysiological markers of ASD, ADHD and ASD+ADHD

REMOVED: Identification of shared and distinct electrophysiological markers of ASD, ADHD and ASD+ADHD

Abstracts / Int. J. Devl Neuroscience 47 (2015) 1–131 ISDN2014 0069 ISDN2014 0070 Identification of shared and distinct electrophysiological markers...

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Abstracts / Int. J. Devl Neuroscience 47 (2015) 1–131

ISDN2014 0069

ISDN2014 0070

Identification of shared and distinct electrophysiological markers of ASD, ADHD and ASD+ADHD

In vivo examination of the relationship between estrogen receptors and microtubule dynamic: A new hypothesis about neuronal degeneration

Charlotte Tye ∗ , Philip Asherson, Karen L. Ashwood, Bahare Azadi, Patrick Bolton, Grainne McLoughlin

Murat Karamese 1,∗ , Selina Aksak Karamese 2 , Emre Karakus 3 , Ozge B. Gundogdu 4 , Bunyami Unal 2

Institute of Psychiatry, King’s College London, United Kingdom E-mail address: [email protected] (C. Tye).

1 Ataturk University, Medical Faculty, Department of Microbiology and Clinical Microbiology, Erzurum 25240, Turkey 2 Ataturk University, Medical Faculty, Department of Histology and Embryology, Erzurum 25240, Turkey 3 Ataturk University, Veterinary Faculty, Department of Pharmacology and Toxicology, Erzurum 25240, Turkey 4 Ataturk University, Medical Faculty, Erzurum 25240, Turkey

There is substantial behavioural and genetic overlap between attention deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD), two common neurodevelopmental disorders that until recently have been largely investigated in separate research fields. In particular both disorders demonstrate attentional and social cognitive deficits, but these have not been directly compared with concurrent electrophysiological (eventrelated potential/ERP) recording that is able to capture the relevant fast occurring cognitive events. Systematically assessed groups of 8-13 year old males with ASD (n = 19), ADHD (n = 18), comorbid ASD+ADHD (n = 29) and typically developing (TD) controls (n = 26) were compared on cognitive-performance data and ERP-indexed brain responses during a cued continuous performance task (CPTOX) and a face/gaze processing task. Results indicate that ERP indices of response inhibition (NoGo-P3) may be altered specifically in children with ADHD, whereas children with ASD show reduced conflict monitoring (Go vs. NoGo-N2) during the CPT-OX. In addition, children with ASD showed atypical lateralisation of the face-sensitive N170 component and altered gaze processing, while children with ADHD showed similar patterns to TD children. While it was possible to dissociate ASD-only and ADHD-only on the basis of cognitive-electrophysiological parameters, across these analyses ASD+ADHD largely show the unique deficits of both disorders, thus supporting an additive co-occurrence of ASD and ADHD. Our findings suggest that disentangling phenotypic variation using neurophysiological markers is likely to aid the identification of susceptibility genes and other causal mechanisms underlying the complex aetiology of ADHD and ASD. In addition, elucidating the basis of comorbidity can help to refine classification systems and enhance the assessment of complex cases for more specific treatment strategies. http://dx.doi.org/10.1016/j.ijdevneu.2015.04.055

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Introduction: Estrogen is one of the most important regulators of neuronal function. There is a broad consensus that loss of estrogen is associated with neurodegeneration in the hippocampus that leads cognitive impairments. Hematopoietic-Pbx-InteractionProtein (HPIP) is a novel scaffolding protein interacts with estrogen receptors and microtubule. Our aim is to explain the new neurodegeneration (axonal-degeneration) model in post-menopausal term and show the possible factors related with this issue. Additionally, we want to show the presence of HPIP, is most likely related with neurodegeneration, in hippocampal neurons first in the world. Methods: A total of 10 female rats were subjected to bilateral ovariectomy. After ovariectomy, the rats were housed for 123 days in a standard laboratory to create menopause model. At the end of the 123 days, the rats were euthanized and the brain sections were investigated by conventional light microscopic and electron microscopic techniques. Real-time-PCR method was used to detect HPIP in neurons. Results: The regular structure of almost all axon extensions was lost. The majority of these extensions had a sawtooth-like appearance in longitudinal section profiles. Especially in transfer section profiles of myelinated axons, some morphological changes were shown which may be matched up with light microscopic findings. According to the results, the mRNA expression of HPIP was found for the first time in hippocampal neurons in the world. Discussion: Deficiency of estrogen will initially affect microtubule organization. When this organization breaks down, it will physically cause the distribution of normal structure of axonal plasmalemma. This in turn will lead to distribution of physical organizations of estrogen and other different types of receptors which are placed in both the membrane and microtubules in the axon. Additionally, a new focus on neurodegeneration in postmenopausal women may arise through the proof of that the HPIP can be found on hippocampal neurons. http://dx.doi.org/10.1016/j.ijdevneu.2015.04.056