Cortical thickness across the cingulate gyrus in schizophrenia and its association to illness duration and memory performance

Schizophrenia has been associated with structural brain abnormalities and cognitive deficits that partly change during the course of illness. In the present study, cortical thickness in five subregions of the cingulate gyrus was assessed in 44 patients with schizophrenia-spectrum disorder and 47 control persons and related to illness duration and memory capacities. In the patients group, cortical thickness was increased in the posterior part of the cingulate gyrus and related to illness duration whereas cortical thickness was decreased in anterior parts unrelated to illness duration. In contrast, cortical thickness was related to episodic and working memory performance only in the anterior but not posterior parts of the cingulate gyrus. Our finding of a posterior cingulate increase may point to either increased parietal communication that is accompanied by augmented neural plasticity or to effects of altered neurodegenerative processes in schizophrenia.

Statistical learning in patients in the minimally conscious state

When listening to an unknown language, listeners could learn the transitional probability between syllables and group frequently co-occurred syllables into a whole unit. Such statistical learning ability has been demonstrated for both pre-verbal infants and adults, even during passive listening. Here, we investigated whether statistical learning occurred in patients in minimally conscious state (MCS) and patients emerged from the minimally conscious state (EMCS) using electroencephalography (EEG). We presented to participants an isochronous sequence of syllables, which were composed of either 2-word real phrases or 2-word artificial phrases that were defined by the transitional probability between words. An inter-trial phase coherence (ITPC) analysis revealed that the phrase-rate EEG response was weakened in EMCS patients compared with healthy individuals, and was even more severely weakened in MCS patients. Although weak, the phrase-rate response or its harmonics remained statistically significant in MCS patients, suggesting that the statistical learning ability was preserved in MCS patients. The word-rate response was also weakened with a decreased level of consciousness. The harmonics of the word-rate response, however,were more salient in MCS than EMCS patients in the alpha and beta bands. Together with previous studies, the current results suggest that MCS patients retain residual learning ability, which can potentially be harnessed to induce neural plasticity, and that different frequency bands are differentially related to the consciousness level.

Repercussion of cAMP and EPAC in Memory and Signaling

It is well recognized that cyclic adenosine monophosphate (cAMP) signaling within neurons plays a key role in the foundation of long-term memories. Memory storage is the process that demands the movement of signals, neural plasticity, and the molecules which can transfer the signals from the sensory neuron to the dorsal root ganglion (DRG) neurons and later into the temporal region of the brain. The discovery of cAMP in 1958 as the second messenger also had a role in memory formation and other neural aspects. Further, in 1998 the scientists found that cAMP does not just activate protein kinase A (PKA) but also exchange protein directly activated by cAMP (Epac) which has an active role to play in hyperalgesia, memory, and signaling. The cAMP has three targets, hyperpolarization-activated cyclic nucleotide modulated (HCN) channels, protein kinase A (PKA), and exchange protein activated by cAMP (Epac). Different research has exposed that both PKA and HCN channels are significant for long-term memory creation. Epac is a cAMP-dependent guanine nucleotide exchange factor for the small G proteins including Rap1. However, slight information is there about the role of Epac in this process. The effects of cAMP are predominantly imparted by activating protein kinase A (PKA) and the more newly discovered exchange proteins are directly activated by cAMP 1 and 2 (EPAC1 and EPAC2). This review provides an insight regarding the function and role of both of these secondary messengers in memory and nerve signaling.

Current criteria for selecting cochlear implant in deaf patients: a review

Cochlear implantation is indicated in patients with severe to profound hearing loss that cannot be adequately treated by other auditory rehabilitation measures. The definitive indication of cochlear implantation is made on the basis of an extensive interdisciplinary clinical, audiological, radiological, and psychological diagnostic work-up. There are numerous changes are happening in cochlear implant candidacy. These have been associated with concomitant changes in surgical techniques, which enhanced the utility and safety of cochlear implantation. Currently, cochlear implants are approved for individuals with severe to profound unilateral hearing loss rather than previously needed for bilateral profound hearing loss. Studies have begun using the short electrode arrays for shallow insertion in patients with low-frequency residual hearing loss. The advancement in designs of the cochlear implant along with improvements in surgical techniques reduce the complications and result in the safety and efficacy of the cochlear implant which further encourages the use of these devices. This review article aims to discuss the new concepts in the candidacy of the cochlear implant, cochlear implant in younger children and hearing preservation, a cochlear implant for unilateral deafness, bilateral cochlear implant, and cochlear implant with neural plasticity and selection of patients for the cochlear implant.

Motor imagery practice and feedback effects on functional connectivity

– Objective: the use of motor imagery (MI) in motor rehabilitation protocols has been increasingly investigated as a potential technique for enhancing traditional treatments, yielding better clinical outcomes. However, since MI performance can be challenging, practice is usually required. This demands appropriate training, actively engaging the MI-related brain areas, consequently enabling the user to properly benefit from it. The role of feedback is central for MI practice. Yet, assessing which underlying neural changes are feedback-specific or purely due to MI practice is still a challenging effort, mainly due to the difficulty in isolating their contributions. In this work, we aimed to assess functional connectivity (FC) changes following MI practice that are either extrinsic or specific to feedback. Approach: to achieve this, we investigated FC, using graph theory, in electroencephalography (EEG) and functional magnetic resonance imaging (fMRI) data, during MI performance and at resting-state (rs), respectively. Thirty healthy subjects were divided into three groups, receiving no feedback (control), “false” feedback (sham) or actual neurofeedback (active). Participants underwent 12 to 13 hands-MI EEG sessions and pre- and post-MI training fMRI exams. Main results: following MI practice, control participants presented significant increases in degree and in eigenvector centrality for occipital nodes at rs-fMRI scans, whereas sham-feedback produced similar effects, but to a lesser extent. Therefore, MI practice, by itself, seems to stimulate visual information processing mechanisms that become apparent during basal brain activity. Additionally, only the active group displayed decreases in inter-subject FC patterns, both during MI performance and at rs-fMRI. Significance: hence, actual neurofeedback impacted FC by disrupting common inter-subject patterns, suggesting that subject-specific neural plasticity mechanisms become important. Future studies should consider this when designing experimental NFBT protocols and analyses.

The MAP Kinase Phosphatase MKP-1 Modulates Neurogenesis via Effects on BNIP3 and Autophagy

Inherited and acquired defects in neurogenesis contribute to neurodevelopmental disorders, dysfunctional neural plasticity, and may underlie pathology in a range of neurodegenerative conditions. Mitogen-activated protein kinases (MAPKs) regulate the proliferation, survival, and differentiation of neural stem cells. While the balance between MAPKs and the family of MAPK dual-specificity phosphatases (DUSPs) regulates axon branching and synaptic plasticity, the specific role that DUSPs play in neurogenesis remains unexplored. In the current study, we asked whether the canonical DUSP, MAP Kinase Phosphatase-1 (MKP-1), influences neural stem cell differentiation and the extent to which DUSP-dependent autophagy is operational in this context. Under basal conditions, Mkp-1 knockout mice generated fewer doublecortin (DCX) positive neurons within the dentate gyrus (DG) characterized by the accumulation of LC3 puncta. Analyses of wild-type neural stem cell (NSC) differentiation in vitro revealed increased Mkp-1 mRNA expression during the initial 24-h period. Notably, Mkp-1 KO NSC differentiation produced fewer Tuj1-positive neurons and was associated with increased expression of the BCL2/adenovirus E1B 19-kD protein-interacting protein 3 (BNIP3) and levels of autophagy. Conversely, Bnip3 knockdown in differentiated Mkp-1 KO NSCs reduced levels of autophagy and increased neuronal yields. These results indicate that MKP-1 exerts a pro-neurogenic bias during a critical window in NSC differentiation by regulating BNIP3 and basal autophagy levels.

Sleep markers in psychiatry: do insomnia and disturbed sleep play as markers of disrupted neuroplasticity in mood disorders? A proposed model

Introduction: Since insomnia and disturbed sleep may affect neuroplasticity, we aimed at reviewing their potential role as markers of disrupted neuroplasticity involved in mood disorders. Method: We performed a systematic review, according to PRIMA, on PubMed, PsycINFO and Embase electronic databases for literature regarding mood disorders, insomnia, sleep loss/deprivation in relation to different pathways involved in the impairment of neuroplasticity in mood disorders such as 1] alterations in neurodevelopment 2] activation of the stress system 3] neuroinflammation 4] neurodegeneration/neuroprogression, 4] deficit in neuroprotection. Results: Sixty-five articles were analyzed and a narrative/ theoretical review was conducted. Studies showed that insomnia, sleep loss and sleep deprivation might impair brain plasticity of those areas involved in mood regulation throughout different pathways. Insomnia and disrupted sleep may act as neurobiological stressors that by over-activating the stress and inflammatory systems may affect neural plasticity causing neuronal damage. In addition, disturbed sleep may favor a deficit in neuroprotection hence contributing to impaired neuroplasticity. Conclusions: Insomnia and disturbed sleep may play a role as markers of alteration in brain plasticity in mood disorders. Assessing and targeting insomnia in the clinical practice may potentially play a neuroprotective role, contributing to “repairing” alterations in neuroplasticity or to the functional recovery of those areas involved in mood and emotion regulation.

Molecular basis of parental contributions to the behavioural tolerance of elevated pCO 2 in a coral reef fish

Knowledge of adaptive potential is crucial to predicting the impacts of ocean acidification (OA) on marine organisms. In the spiny damselfish, Acanthochromis polyacanthus , individual variation in behavioural tolerance to elevated pCO 2 has been observed and is associated with offspring gene expression patterns in the brain. However, the maternal and paternal contributions of this variation are unknown. To investigate parental influence of behavioural pCO 2 tolerance, we crossed pCO 2 -tolerant fathers with pCO 2 -sensitive mothers and vice versa, reared their offspring at control and elevated pCO 2 levels, and compared the juveniles' brain transcriptional programme. We identified a large influence of parental phenotype on expression patterns of offspring, irrespective of environmental conditions. Circadian rhythm genes, associated with a tolerant parental phenotype, were uniquely expressed in tolerant mother offspring, while tolerant fathers had a greater role in expression of genes associated with histone binding. Expression changes in genes associated with neural plasticity were identified in both offspring types: the maternal line had a greater effect on genes related to neuron growth while paternal influence impacted the expression of synaptic development genes. Our results confirm cellular mechanisms involved in responses to varying lengths of OA exposure, while highlighting the parental phenotype's influence on offspring molecular phenotype.

Endurance exercise ameliorates phenotypes in Drosophila models of Spinocerebellar Ataxias

Endurance exercise is a potent intervention with widespread benefits proven to reduce disease incidence and impact across species. While endurance exercise supports neural plasticity, enhanced memory, and reduced neurodegeneration, less is known about the effect of chronic exercise on the progression of movement disorders such as ataxias. Here, we focused on three different types of ataxias, Spinocerebellar Ataxias Type (SCAs) 2, 3, and 6, belonging to the polyglutamine (polyQ) family of neurodegenerative disorders. In Drosophila models of these SCAs, flies progressively lose motor function. Here, we observe marked protection of speed and endurance in exercised SCA2 flies and modest protection in exercised SCA6 models, while no benefit is observed in SCA3 flies. Causative protein levels are reduced in SCA2 flies after chronic exercise, but not in SCA3 models, linking protein levels to exercise-based benefits. Additional investigations indicate that the exercise-inducible protein, Sestrin (Sesn) suppresses mobility decline and improves early death in SCA2 flies, even without exercise, coincident with disease protein level reduction and increased autophagic flux. These improvements depend on previously established functions of Sesn that reduce oxidative damage and modulate mTOR activity. Our study suggests differential responses of polyQ SCAs to exercise, highlighting the potential for more extensive application of exercise-based therapies in the prevention of polyQ neurodegeneration. Defining the mechanisms by which endurance exercise suppresses polyQ SCAs will open the door for more effective treatment for these diseases.