Neuroscience
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The neural mechanisms associated with the limited capacity of working memory (WM) has long been studied, but it is still unclear which neural regions are associated with the precision of visual WM. Here, an orientation recall task for estimating the trial-wise precision of visual WM was performed and then repeated two weeks later in an fMRI scanner. Results showed that activity in frontal and parietal regions during WM maintenance scaled with WM load, but not with the precision of WM (i.e., recall error in radians). ⋯ Interestingly, a region within the prefrontal cortex, the inferior frontal junction (IFJ), exhibited greater functional connectivity with LOC when the WM load increased. Together, our findings provide unique evidence that the LOC supports visual WM precision, while communication between the IFJ and LOC varies based on WM load demands. These results suggest an intriguing possibility that distinct neural mechanisms may be associated with general content (load) or detailed information (precision) of WM.
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Mechanisms of Impulsive Responding to Temporally Predictable Events as Revealed by Electromyography.
Temporal predictability optimises behaviour when a simple response is required, as demonstrated by faster reaction times (RTs) and higher accuracy. However, its beneficial effects come at a cost under situations of response conflict. Here, we investigated the motor underpinnings of behaviour to temporally predictable events in the Simon conflict task. ⋯ There was, however, no effect of temporal predictability on subsequent suppression of partial errors. Our results provide direct evidence that temporal predictability acts by increasing the urge to initiate a fast, yet potentially erroneous, response. This mechanism parsimoniously explains both beneficial effects of temporal predictability when no conflict in the environment is present, as well as its costs when more complex motor behaviour is required.
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The number of patients suffering from dementia due to Alzheimer's disease (AD) is constantly rising worldwide. This has accordingly resulted in huge burdens on the health systems and involved families. Lack of profound understanding of neural networking in normal brain and their interruption in AD makes the treatment of this neurodegenerative multifaceted disease a challenging issue. ⋯ Application of the graph theoretical analysis in the brain imaging was reviewed, depicting the relations between brain structure and function, without diving into mathematical details. Moreover, differential rate equations were briefly articulated, emphasizing the potential use of these equations in simplifying complex processes in relevance to pathologies of AD. Comprehensive insights were given into the AD progression from neural networks perspective, which may lead us towards potential strategies for early diagnosis and effective treatment of AD.
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Fluoro-Jade C (FJC) staining is widely used for the specific detection of all degenerating mature neurons, including apoptotic, necrotic, and autophagic cells. However, whether FJC staining can detect degenerating immature neurons and neural stem/precursor cells remains unclear. In addition, some conflicting studies have shown that FJC and its ancestral dyes, Fluoro-Jade (FJ) and FJB, can label resting/activated astrocytes and microglia. ⋯ Surprisingly degenerating mesenchymal cells were also FJC(+). The present study indicates that FJC is a reliable marker for degenerating neuronal cells during all differentiation stages. However, FJC could also label degenerating non-neuronal cells under some conditions.
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In several tauopathies such as Alzheimer's disease (AD), an increased incidence of seizures is observed. Tau, one of the major proteins implicated in AD pathology, is an important regulator of neural network excitability and might participate in the underlying epileptic cascade. However, the mechanisms underlying this relationship are not fully elucidated. ⋯ Also, age-related differences in susceptibility could be demonstrated for both genotypes. Identification and targeting of secondary diseases such as epilepsy, which aggravate dementia and lead to earlier institutionalization, is key. This study finds that tau pathology itself is sufficient to alter seizure susceptibility in a rodent model, indicating that the disease process is crucial in the emergence of epilepsy in patients with tauopathy.