Difficulties Faced by Special Education Teachers during COVID-19 Pandemic

The purpose of this research is to find out what difficulties special education instructors’ face when it comes to educating children with special needs during the COVID-19 pandemic. Participants in this research were 30 special education instructors who were chosen through a purposive sampling procedure to serve as respondents. In order to identify the difficulties and challenges faced by special education instructors, both quantitative and qualitative techniques were used. In an attempt to comprehend the data, a descriptive analysis was performed. During the COVID-19 pandemic, special education instructors who worked with students who had learning impairments did not get any technology assistance in order to educate the students. According to the findings of the research, the instructional method for special learners has a suboptimal learning environment as a result of the absence of web-based instructional teaching. The survey's major findings identified 15 difficulties, with the most significant of these being 'insufficient e-learning resources', 'lack of training for online teaching', 'giving feedback to students', and 'making the students to attend online classes', as per survey respondents. According to the results, practitioners and curriculum designers may use the information to build and improve the special education system, teaching techniques, and technologically imbibed instructional learning among special education instructors.

Potential of Sorghum Polyphenols to Prevent and Treat Alzheimer’s Disease: A Review Article

Alzheimer’s disease (AD) is characterized by the excessive deposition of extracellular amyloid-beta peptide (Aβ) and the build-up of intracellular neurofibrillary tangles containing hyperphosphorylated tau proteins. This leads to neuronal damage, cell death and consequently results in memory and learning impairments leading to dementia. Although the exact cause of AD is not yet clear, numerous studies indicate that oxidative stress, inflammation, and mitochondrial dysfunction significantly contribute to its onset and progression. There is no effective therapeutic approach to stop the progression of AD and its associated symptoms. Thus, early intervention, preferably, pre-clinically when the brain is not significantly affected, is a better option for effective treatment. Natural polyphenols (PP) target multiple AD-related pathways such as protecting the brain from Aβ and tau neurotoxicity, ameliorating oxidative damage and mitochondrial dysfunction. Among natural products, the cereal crop sorghum has some unique features. It is one of the major global grain crops but in the developed world, it is primarily used as feed for farm animals. A broad range of PP, including phenolic acids, flavonoids, and condensed tannins are present in sorghum grain including some classes such as proanthocyanidins that are rarely found in others plants. Pigmented varieties of sorghum have the highest polyphenolic content and antioxidant activity which potentially makes their consumption beneficial for human health through different pathways such as oxidative stress reduction and thus the prevention and treatment of neurodegenerative diseases. This review summarizes the potential of sorghum PP to beneficially affect the neuropathology of AD.

Reward-Based Reinforcement Learning in Altered Among Individuals with a History of Major Depressive Disorder and Psychomotor Retardation Symptoms

Background: Reward-based reinforcement learning impairments are common in major depressive disorder, but it is unclear which reward-based reinforcement learning is disrupted in remitted major depression (rMDD). As the neurobiological substrates that implement reward-based RL are also strongly implicated in psychomotor retardation (PmR), the present study sought to test whether reward-based reinforcement learning is particularly altered in rMDD individuals with past PmR. Methods: Three groups of individuals (1) rMDD with past PmR (PmR+, N=34), rMDD without past PmR (PmR-, N=44) and healthy controls (N=90) completed a reward-based reinforcement learning task. Computational modeling was applied to test for group differences in model-derived parameters – specifically, learning rate, reward sensitivity, and value estimates. Results: Compared to controls, rMDD PmR + exhibited lower learning rates, but not reduced reward sensitivity. Relative to rMDD PmR-, rMDD PmR + exhibited reduced value estimation early, but not later, in the reinforcement learning task. Follow-up analyses indicated that the results were not due to current psychopathology symptoms.Conclusions: Results indicate that a history of PmR predicts altered reward-based reinforcement learning in rMDD. Abnormal reward-related reinforcement learning may reflect a scar of past depressive episodes that contained psychomotor symptoms, or a trait-like deficit that preceded these episodes.

Culture of collaboration

Purpose: The purpose of this article is to report the results from a research project which focused on understanding how motivation to read is manifested and maintained in children with learning impairments. The participants were enrolled in a specialized university literacy program with graduate student clinicians. Method: An interpretative, qualitative study utilizing components of ethnography and microanalysis was employed to analyze video transcripts of recorded therapy sessions of speech-language pathology student clinicians and children with language disorders. These interactions were coded for the nature of their role in motivating children to read. Results and conclusions: This study revealed that a culture of collaboration was a hallmark of treatment that facilitated motivation in the participants. Two key characteristics of motivated behavior that emerged as a result of this culture of collaboration are identified and described. Additionally, three specific, collaborative, therapeutic strategies found to sustain motivation to read are described.

Adulthood Deficiency of the Insulin-like Growth Factor-1 Receptor in Hippocampal Neurons Impairs Cell Structure and Spatial Learning and Memory in Male and Not Female Mice

Reductions in insulin-like growth factor-1 (IGF-1) are associated with cognitive impairment and increased risk of neurodegenerative disease in advanced age. In mouse models, reduced IGF-1 early-in-life leads to memory impairments and synaptic dysfunction; however, these models are limited by systemic reductions in IGF-1. We hypothesized that IGF-1 continues to promote hippocampal neuron structure and function after development, and as such, the loss of IGF-1 signaling in adult neurons would lead to impaired spatial learning and memory. To test this, the IGF-1 receptor (IGF-1R) was genetically targeted in hippocampal neurons of adult male and female mice. Male mice deficient in neuronal IGF-1R exhibited spatial learning impairments as evidenced by increased pathlength and errors in the radial arm water maze. No differences in learning and memory were observed in female mice. Golgi-Cox staining revealed a reduced number of dendritic boutons of neurons the CA1 region of the hippocampus in male mice. Decreased MAPK and increased ROCK activity were also observed in these tissues. In vitro studies revealed that impaired neurite outgrowth due to inhibited IGF-1R signaling could be rescued by pharmacological inhibitors of ROCK. However, ROCK inhibition in neuronal IGF-1R deficient mice did not fully rescue learning impairments or bouton numbers. Together, our study highlights that IGF-1 continues to support spatial learning and memory and neuronal structure in adulthood.

Mechanistic and Efficacy Study on Effects of Fibroin Enzymatic Hydrolysate (FEH) on Memory and Learning Impairments Induced by Scopolamine in Mice

In addition, FEH treatment increased ACh and BDNF levels, and reduced the levels of IL-1β, TNF-α and IL-6 in brain hippocampal tissue of mice with scopolamine-induced memory and learning impairment. Furthermore, FEH treatment enhanced the expression of phosphorylated cAMP response element-binding protein (p-CREB) and BDNF via the stimulation of the phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin/postsynaptic density protein 95 (p-PI3K/p-AKT/mTOR/PSD95) pathway, and activation of Extracellular Signal-Regulated Kinases (ERK) and Ca2+/calmodulin-dependent protein kinase II (CaMKII). These results provide extensive information regarding the protective mechanism of action of FEH, and support the potential of FEH supplementation to prevent learning and memory impairment.

Intrahippocampal co-administration of nicotine and O-acetyl-L-carnitine prevents the H-89-induced spatial learning deficits in Morris water maze

Objectives H-89 (a protein kinase AII [PKA II] inhibitor) impairs the spatial memory in the Morris water maze task in rats. In the present study, we aimed to study the protective effects of nicotine and O-acetyl-L-carnitine against H-89-induced spatial memory deficits. Methods Spatial memory impairment was induced by the bilateral intrahippocampal administration of 10 µM H-89 (dissolved in dimethyl sulfoxide, DMSO) to rats. The rats then received bilateral administrations of either nicotine (1 μg/μL, dissolved in saline) or O-acetyl-L-carnitine (100 μM/side, dissolved in deionized water) alone and in combination. Control groups received either saline, deionized water, or DMSO. Results The H-89-treated animals showed significant increases in the time and distance travelled to find hidden platforms, and there was also a significant decrease in the time spent in the target quadrant compared to DMSO-treated animals. Nicotine and O-acetyl-L-carnitine had no significant effects on H-89-induced spatial learning impairments alone, but the bilateral intrahippocampal co-administration of nicotine and O-acetyl-L-carnitine prevented H-89-induced spatial learning deficits and increased the time spent in the target quadrant in comparison with H-89-treated animals. Conclusions Our results indicated the potential synergistic effects of nicotine and O-acetyl-L-carnitine in preventing protein kinase AII inhibitor (H-89)-induced spatial learning impairments.