Journal of Neuroscience Research最新文献

Epilepsy is a common neurological disorder of great importance to patients and society. Sclerosis is associated with neuronal loss and neurodegeneration in specific regions of the hippocampal formation. The hippocampal formation and temporal lobe are not the only regions affected; the chronicity of the disease extends the involvement to other brain regions. Our aim is to investigate the spatial relationship of anatomical structures in both control (CO) and epileptic (EP) subjects using magnetic resonance imaging (MRI) in order to determine changes in epileptic patients compared to healthy anatomical structures. Anatomical landmarks are identified and registered in 3D space to provide a reference for the brain structures; the 3D network is described quantitatively using planar distances, as well as measuring rostrocaudal and Euclidean distances. The planar and rostrocaudal distances are the most remarkable discriminators between CO and EP groups, especially between structures located in and outside the temporal lobe. The study achieves a 100% discrimination between the control group and the epileptic group with the discriminant use of two distances: D_PL, Hpe/Cde and D_RC, As/cae. Finally, discriminates 100% between the three study groups, control group CO, extratemporal lobe epilepsy ETLE and temporal lobe epilepsy TLE, with a total of 12 distances distributed in the three axes of space. This study allows us to hope for a future application, its clinical utility may allow us not only to identify processes (in our case, epilepsy), but also to obtain parameters of the evolution of the disease.

Human induced pluripotent stem cells (hiPSCs), similar to embryonic stem cells, are a class of pluripotent stem cells with the potential to differentiate into various kinds of cells. Because the application of hiPSCs obtained by reprogramming patients' somatic cells in the treatment of brain diseases bypasses the ethical constraints on the use of embryonic stem cells and mitigates immune rejection, hiPSCs have profound clinical application prospects. In this review, we first summarized the differentiation methods of hiPSCs into different kinds of neurons, and secondly discussed the application of hiPSCs in several brain disease models, so as to provide a reference for the future application of hiPSCs in the studies and treatment of brain diseases.

Chronic stress is a common trigger of multiple neuropsychiatric illnesses. Animal models are widely used to study stress-induced brain disorders and their interplay with neuroinflammation and other neuroimmune processes. Here, we apply the prolonged 12-week chronic unpredictable stress (PCUS) model to examine rat behavioral and hippocampal transcriptomic responses to stress and to chronic 4-week treatment with a classical antidepressant fluoxetine, an anti-inflammatory agent eicosapentaenoic acid (EPA), a pro-inflammatory agent lipopolysaccharide and their combinations. Overall, PCUS evoked anxiety-like behavioral phenotype in rats, corrected by chronic fluoxetine (alone or combined with other drugs), and EPA. PCUS also evoked pronounced transcriptomic responses in rat hippocampi, involving > 200 differentially expressed genes. While pharmacological manipulations did not affect hippocampal gene expression markedly, Gpr6, Drd2 and Adora2a were downregulated in stressed rats treated with fluoxetine, EPA and fluoxetine + EPA, suggesting their respective protein products (G protein-coupled receptor 6, dopamine D2 receptor and adenosine A2A receptor) as potential evolutionarily conserved targets under chronic stress. Overall, these findings support the validity of rat PCUS paradigm as a useful model to study stress-related anxiety pathogenesis, and call for further research probing how various conventional and novel drugs may (co)modulate behavioral and neurotranscriptomic biomarkers of chronic stress.

Parkinson's disease (PD)-related depression is associated with aberrant neuronal oscillations and 5-hydroxytryptamine (5-HT) neurotransmission in the medial prefrontal cortex (mPFC). Intermittent theta-burst stimulation (iTBS), an updated pattern of high-frequency repetitive transcranial magnetic stimulation, has possible efficacy in PD-related depression. However, whether iTBS alleviates PD-related depression through modulating neuronal oscillations and 5-HT levels in the mPFC has not been determined. In this study, male Sprague–Dawley rats were used to establish a unilateral 6-hydroxydopamine-induced PD model. Then, acute iTBS was applied to the parkinsonian rats, and behavioral, neurochemical, and electrophysiological experiments were performed. We found that the parkinsonian rats exhibited increased immobility time and decreased sucrose preference accompanied by an increase of δ power and a decrease of θ power in the mPFC compared to sham-operated rats. One block of iTBS (1 block-iTBS, 300 stimuli) alleviated depressive-like behaviors in parkinsonian rats and elevated 5-HT levels in the mPFC compared to sham-iTBS. Additionally, it altered neuronal oscillations in the mPFC in the opposite fashion by suppressing the δ rhythm and enhancing the θ and β rhythms compared to sham-iTBS, suggesting that acute iTBS induces hyperactivity in the mPFC. With this iTBS paradigm, we also observed decreased parvalbumin expression in the mPFC, reflecting reduced cortical inhibition. Finally, correlation analyses showed strong correlation between immobility time and θ power after 1 block-iTBS. These findings suggest that the application of acute iTBS in parkinsonian rats produces antidepressant-like effects, which may be associated with elevated 5-HT levels and normalized neuronal oscillations in the mPFC.

In studying the neural correlates of working memory (WM) ability via functional magnetic resonance imaging (fMRI) in health and disease, it is relatively uncommon for investigators to report associations between brain activation and measures of task performance. Additionally, how the choice of WM task impacts observed activation–performance relationships is poorly understood. We sought to illustrate the impact of WM task on brain–behavior correlations using two large, publicly available datasets. We conducted between-participants analyses of task-based fMRI data from two publicly available datasets: The Human Connectome Project (HCP; n = 866) and the Queensland Twin Imaging (QTIM) Study (n = 459). Participants performed two distinct variations of the n-back WM task with different stimuli, timings, and response paradigms. Associations between brain activation ([2-back − 0-back] contrast) and task performance (2-back % correct) were investigated separately in each dataset, as well as across datasets, within the dorsolateral prefrontal cortex (dlPFC), medial prefrontal cortex, and whole cortex. Global patterns of activation to task were similar in both datasets. However, opposite associations between activation and task performance were observed in bilateral pre-supplementary motor area and left middle frontal gyrus. Within the dlPFC, HCP participants exhibited a significantly greater activation–performance relationship in bilateral middle frontal gyrus relative to QTIM Study participants. The observation of diverging activation–performance relationships between two large datasets performing variations of the n-back task serves as a critical reminder for investigators to exercise caution when selecting WM tasks and interpreting neural activation in response to a WM task.

The primary objective of this study was to examine neurological disorders and cognitive impairments in patients with secondary hypothyroidism and epilepsy undergoing treatment with antiepileptic medications. The study included 184 patients divided into three groups: Group 1 (subclinical hypothyroidism, n = 60), Group 2 (manifest hypothyroidism, n = 64), and Group 3 (control, n = 60). Patients in Group 2 received levothyroxine therapy (initial dose of 25 μg/day, titrated to 50–100 μg/day), while Groups 1 and 2 were treated with anti-seizure medications (valproic acid, 40 mg/kg/day). Neurological symptoms, including Babinski's reflex abnormalities (χ² = 8.15, p = 0.017) and sensory disturbances (χ² = 12.44, p = 0.005), were significantly more frequent in Group 2 than in Group 1. Cognitive test scores were significantly lower in Group 2 compared to Group 3 across all domains (F(2, 181) = 6.55, p = 0.002 for MMSE; F(2, 181) = 4.70, p = 0.010 for FAB; and F(2, 181) = 5.75, p = 0.006 for CDT), with Group 1 showing intermediate results. Regression analysis identified neurodegenerative disease risk (β = 0.34, CI: 0.20–0.48, p < 0.001), anemia (β = 0.32, CI: 0.15–0.49, p = 0.001), and prolonged stress (β = 0.26, CI: 0.12–0.40, p = 0.002) as significant predictors of cognitive decline, while higher education was protective (β = −0.28, CI: −0.42 to −0.14, p = 0.003). An inverse relationship was observed between TSH levels and cognitive scores (r = −0.55, p < 0.001).