Neuroscience
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Neurodegenerative and demyelinating disease, such as multiple sclerosis (MS) are at the forefront of medical research and the discovery of new drugs and therapeutics. One phenomenon of degeneration seen in these diseases is transsynaptic degeneration (TSD), where damage from one axon spreads to the other axons that are connected to it synaptically. It has previously been found that demyelination occurs prior to neuronal loss in an experimental form of induced TSD. ⋯ Most notably, 9CDHRA was able to maintain myelin levels following ONC, and effectively protected from demyelination. This was corroborated by VEP recordings with improved P1 latency. The promising findings regarding the injury attenuating and myelin protecting properties of 9CDHRA necessitates further investigations into the potential therapeutic uses of this compound.
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The aim of this study was to assess the potential causal relationship between neuroticism and 12 neuroticism items with intracranial aneurysms (IAs) and aneurysmal subarachnoid hemorrhage (aSAH) using a two-sample Mendelian randomization (MR) approach. ⋯ Our Mendelian randomization analysis demonstrated genetic causality between neuroticism and neuroticism items with intracranial aneurysms, aneurysmal subarachnoid hemorrhage, and unruptured intracranial aneurysms, and further studies are needed to confirm these results and explore potential mechanisms of action.
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Previous studies showed that women with gestational diabetes mellitus (GDM) are susceptible to cognitive dysfunction. We investigated the effects of GDM on brain pathologies and premature brain aging in rats. Seven-week-old female Sprague-Dawley rats were fed a normal diet (ND) or a high-fat diet (HFD) after two weeks of acclimatization. ⋯ On postpartum day 21, brains and blood were collected. The GDM group showed increased inflammatory and premature aging markers, mitochondrial changes, and compensatory increases in the blood-brain barrier and synaptic proteins in the prefrontal cortex and hippocampus. GDM triggers maternal brain inflammation and premature aging, suggesting compensatory mechanisms may protect against these effects.
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Increasing evidence demonstrates that brain-derived neurotrophic factor (BDNF) can be regarded as a biomarker for major depression. Our previous work found that the ratio of mature BDNF (mBDNF) to precursor-BDNF (proBDNF) was a pivotal factor in the pathogenesis of major depressive disorder (MDD). But the mechanism behind the ratio is still obscure. ⋯ The combination of tPA + PAI + BDNF showed the best diagnostic value for MDD. In summary, our data suggested that the interaction between tPA and PAI-1 implicated to the MDD and the antidepressant treatment which might through regulating the BDNF/proBDNF ratio. The combination of tPA, PAI-1 and BDNF might offer a helpful way for MDD diagnosis.
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Anhedonia is one of the core features of the negative symptoms of schizophrenia and can be extremely burdensome. Our study applied resting-state functional magnetic resonance imaging (fMRI)-based support vector regression (SVR) to predict anhedonia in patients with first-episode schizophrenia (FES) and analysed the correlation between the wavelet-based amplitude low-frequency fluctuation (wavelet-ALFF) of the main brain region and anhedonia. We recruited 31 patients with FES and 33 healthy controls (HCs) from the Affiliated Brain Hospital of Guangzhou Medical University. ⋯ The SVR analysis showed that wavelet-ALFF, based primarily on the right putamen (r = 0.40, P<0.05) and right superior occipital gyrus (r = -0.39, P<0.05), was effective in predicting consummatory pleasure scores with an accuracy of 56.43 %. Our study shows that abnormal spontaneous neural activity in FES may be related to the state of consummatory anhedonia in FES. Wavelet-ALFF changes in the right putamen and superior occipital gyrus may be a biological feature of FES with anhedonia and could serve as a potential biological marker of FES with anhedonia.