49 research outputs found

    Interoception in anxiety and depression

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    We review the literature on interoception as it relates to depression and anxiety, with a focus on belief, and alliesthesia. The connection between increased but noisy afferent interoceptive input, self-referential and belief-based states, and top-down modulation of poorly predictive signals is integrated into a neuroanatomical and processing model for depression and anxiety. The advantage of this conceptualization is the ability to specifically examine the interface between basic interoception, self-referential belief-based states, and enhanced top-down modulation to attenuate poor predictability. We conclude that depression and anxiety are not simply interoceptive disorders but are altered interoceptive states as a consequence of noisily amplified self-referential interoceptive predictive belief states

    The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Abeta protofibril formation.

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    Several pathogenic Alzheimer's disease (AD) mutations have been described, all of which cause increased amyloid beta-protein (Abeta) levels. Here we present studies of a pathogenic amyloid precursor protein (APP) mutation, located within the Abeta sequence at codon 693 (E693G), that causes AD in a Swedish family. Carriers of this 'Arctic' mutation showed decreased Abeta42 and Abeta40 levels in plasma. Additionally, low levels of Abeta42 were detected in conditioned media from cells transfected with APPE693G. Fibrillization studies demonstrated no difference in fibrillization rate, but Abeta with the Arctic mutation formed protofibrils at a much higher rate and in larger quantities than wild-type (wt) Abeta. The finding of increased protofibril formation and decreased Abeta plasma levels in the Arctic AD may reflect an alternative pathogenic mechanism for AD involving rapid Abeta protofibril formation leading to accelerated buildup of insoluble Abeta intra- and/or extracellularly

    Perception Abilities of L1 Cypriot Greek Listeners - Types of Errors Involving Plosive Consonants in L2 English

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    This paper investigates the difficulties adult second language (L2) users of English encounter with plosive consonants in the L2. It presents the results of a task examining the acquisition of plosive voicing contrasts by college students with Cypriot Greek (CG) linguistic background. The task focused on the types of errors involving plosive consonants indicating that performance was significantly better in the voiceless plosive category. Participants were able to perceive voiced plosives but they treated such instances as a /nasal + voiced plosive/ sequence. Therefore, the question raised concerns different phonological contrasts realised through similar phonetic cues. The patterns observed suggested that this gap between phonetic cues and phonological contrast might explain why CG users have difficulties perceiving voiced English plosives. In this context, voice onset time (VOT) differences between the L1 and L2 are of crucial importance. In English, voiced plosives are characterised by short lag VOT while their voiceless counterparts fall within the long lag VOT continuum. The same phonetic contrast is used in CG to differentiate between single and geminate voiceless plosives. The results are discussed in relation to the frameworks of second language phonology and speech perception suggesting that the difficulties faced by the L2 listeners support the operation of a phonetic-phonological challenge. © 2016 Springer Science+Business Media New Yor

    Impaired synaptic plasticity and learning in aged APP transgenic mice

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    We investigated synaptic communication and plasticity in hippocampal slices from mice overexpressing mutated 695-amino-acid human amyloid precursor protein (APP695SWE), which show behavioral and histopathological abnormalities simulating Alzheimer's disease. Although aged APP transgenic mice exhibit normal fast synaptic transmission and short term plasticity, they are severely impaired in in-vitro and in-vivo long-term potentiation (LTP) in both the CA1 and dentate gyrus regions of the hippocampus. The LTP deficit was correlated with impaired performance in a spatial working memory task in aged transgenics. These deficits are accompanied by minimal or no loss of presynaptic or postsynaptic elementary structural elements in the hippocampus, suggesting that impairments in functional synaptic plasticity may underlie some of the cognitive deficits in these mice and, possibly, in Alzheimer's patients
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