Specific Learning Disabilities and Psychosocial Difficulties in Children

Children with specific learning disorders (SLDs) exhibit academic difficulties disproportional to their intellectual capabilities. A significant percentage of school-aged children worldwide are diagnosed with specific learning disabilities, with dyslexia being the most common. In Greece, epidemiological data propose that 50% of children in special education schools are diagnosed with learning disabilities, and 80% with reading difficulties. Children with SLD exhibit both internalized, such as depressive and anxiety disorders, self-esteem issues, eating and sleep difficulties, and externalized problems, including difficulties in socializing, developing friendships, and delinquent behavior. Moreover, research has shown that children with learning disabilities have an average (or above average) intelligence, and their poor academic performance is due to their lack of effective learning strategies. Concerning cognitive deficiencies, research suggests that no specific deficit is to fault; however, common deficits in children with SLDs are phonological processing and working memory.

Transferring cognitive talent across domains to reduce the disposition effect in investment

We consider Theory of Mind (ToM), the ability to correctly predict the intentions of others. To an important degree, good ToM function requires abstraction from one’s own particular circumstances. Here, we posit that such abstraction can be transferred successfully to other, non-social contexts. We consider the disposition effect, which is a pervasive cognitive bias whereby investors, including professionals, improperly take their personal trading history into account when deciding on investments. We design an intervention policy whereby we attempt to transfer good ToM function, subconsciously, to personal investment decisions. In a within-subject repeated-intervention laboratory experiment, we record how the disposition effect is reduced by a very significant 85%, but only for those with high scores on the social-cognitive dimension of ToM function. No such transfer is observed in subjects who score well only on the social-perceptual dimension of ToM function. Our findings open up a promising way to exploit cognitive talent in one domain in order to alleviate cognitive deficiencies elsewhere.

Trimethylamine N-Oxide (TMAO) links peripheral insulin resistance and cognitive deficiencies in a senescence accelerated mouse model

It has been established that ageing is the major risk factor for cognitive deficiency or neurodegenerative diseases such as Alzheimer's disease (AD) and it is becoming increasingly evident that insulin resistance is another factor. Biological plausibility for a link between insulin resistance and dementia is relevant for understanding disease etiology, and to form bases for prevention efforts to decrease disease burden. The dysfunction of the insulin signaling system and glucose metabolism has been proposed to be responsible for brain aging. Normal insulin signaling in the brain is required to mediate growth, metabolic functions, and the survival of neurons and glia. Insulin receptors are densely expressed in the olfactory bulb, the cerebral cortex and the hippocampus and regulate neurotransmitter release and receptor recruitment. In normal elderly individuals, reduced glucose tolerance and decreased insulin levels in the aged brain are typically observed. Furthermore, insulin signaling is aberrantly activated in the AD brain, leading to non-responsive insulin receptor signaling. The senescence accelerated mouse (SAMP8) mouse was one of the accelerated senescence strains that spontaneously developed from breeding pairs of the AKR/J series. The SAMP8 mouse develops early learning and memory deficits (between 6 and 8 months) together with other characteristics similar to those seen in Alzheimer's disease. The present project proposes the investigation of the missing link between aging, insulin resistance and dementia. Peripheral but not central insulin resistance was found in SAMP8 mice accompanied by cognitive deficiencies. Furthermore, a marked peripheral inflammatory state (i.e. significantly higher adipose tissue TNF-[alpha]; and IL6 levels) were observed in SAMP8 mice, followed by neuroinflammation that could be due to a higher cytokine leaking into the brain across a aging-disrupted BBB. Moreover, aging-induced gut dysbiosis produces higher TMAO that could also contribute to the peripheral and central inflammatory tone as well as to the cognitive deficiencies observed in SAMP8 mice. All those alterations were reversed by DMB, a treatment inhibits the transformation of choline, carnitine and crotonobetaine, decreaseing TMAO levels. The ever-increasing incidence of neurodegenerative diseases not only limits the life quality of the affected individuals and their families but also poses an enormous demand on the societies. Thus, it is instrumental to pursue novel promising approaches to prevent and treat it at the highest possible speed to rapidly translate them to clinical practice. From this point of view, data obtained from this project will be instrumental to validate the principle approach of microbial dysbiosis and increased TMAO secretion as a key link between aging, insulin resistance and dementia. Collectively, the proposed experiments ideally integrate the aim to promote a novel approach to improve the lives of those suffering from cognitive disturbances.

Depression and Conversion to Dementia in Mild Cognitive Impairment

Mild cognitive impairment (MCI) is a stage of aging that occurs between normal aging and dementia (precedes dementia). Patients with MCI have memory loss who is otherwise functioning normally and does not match the clinical diagnosis criteria for dementia. MCI is frequently accompanied by cognitive deficits and non-cognitive. One of the most frequent non-cognitive deficiencies is depression. Depression and mild cognitive impairment are closely associate particularly in the elderly and can progress into neurodegenerative disorders like dementia. This indicates that there is a connection that needs to be explored further. Through this review article, a theoretical review of the relationship between MCI with depression and its conversion to dementia.

Transferring Cognitive Talent Across Domains: The Case of Finance

We consider Theory of Mind, the ability to correctly predict the intentions of others. The skill requires abstraction from one’s own particular circumstances. Here, we posit that such abstraction can be transferred successfully to other, non-social contexts. We consider the disposition effect, which is a pervasive cognitive bias whereby investors, including professionals, improperly take their personal trading history into account when deciding on investments. We design an intervention policy whereby we attempt to transfer Theory of Mind skills, subconsciously, to personal investment decisions. In a within-subject repeated-intervention laboratory experiment, we record how the disposition effect is reduced by a very significant 85%, but only for those with high Theory of Mind skills. No such transfer is observed in subjects who score well only on the emotional dimension of interpersonal skills. Our findings open up a promising way to exploit cognitive talents in one domain in order to alleviate cognitive deficiencies elsewhere.

Transferring Cognitive Talent Across Domains: The Case of Finance

We consider Theory of Mind, the ability to correctly predict the intentions of others. The skill requires abstraction from one’s own particular circumstances. Here, we posit that such abstraction can be transferred successfully to other, non-social contexts. We consider the disposition effect, which is a pervasive cognitive bias whereby investors, including professionals, improperly take their personal trading history into account when deciding on investments. We design an intervention policy whereby we attempt to transfer Theory of Mind skills, subconsciously, to personal investment decisions. In a within-subject repeated-intervention laboratory experiment, we record how the disposition effect is reduced by a very significant 85%, but only for those with high Theory of Mind skills. No such transfer is observed in subjects who score well only on the emotional dimension of interpersonal skills. Our findings open up a promising way to exploit cognitive talents in one domain in order to alleviate cognitive deficiencies elsewhere.

Cognitive Deficiencies pathophysiology are mainly an unknown area. Curing the neurological conditions could be an objective for gene therapy

Currently, it appears that the pathophysiology of Cognitive Deficiency (CD) is mostly uncharted territory. In this study, we used both clinical research and mouse models to identify the reported Systemic lupus erythematosus (SLE) symptoms and to explain how tissue damage occurs in SLE, which helps us develop optimal therapies for CD. The primary goal of treatment is to cure the neurological problem, rather than repair the immunological issues. It should be noted that CD develops even in the absence of flares, indicating that treating it would need much more intensive immunosuppression with more damage. For further study on CD, it will be necessary to collaborate amongst neurologists, rheumatologists, and immunologists. This work would succeed by advancing the ability to unveil or hide the fundamental mechanism of CD.

Traffic noise disrupts vocal development and suppresses immune function

Noise pollution has been linked to learning and language deficits in children, but the causal mechanisms connecting noise to cognitive deficiencies remain unclear because experimental models are lacking. Here, we investigated the effects of noise on birdsong learning, the primary animal model for vocal learning and speech development in humans. We found that traffic noise exposure retarded vocal development and led to learning inaccuracies. In addition, noise suppressed immune function during the sensitive learning period, indicating that it is a potent stressor for birds, which is likely to compromise their cognitive functions. Our results provide important insights into the consequences of noise pollution and pave the way for future studies using birdsong as an experimental model for the investigation of noise-induced learning impairments.

Gut Microbiota Alterations and Cognitive Impairment Are Sexually Dissociated in a Transgenic Mice Model of Alzheimer’s Disease

Background: Normal aging is accompanied by cognitive deficiencies, affecting women and men equally. Aging is the main risk factor for Alzheimer’s disease (AD), with women having a higher risk. The higher prevalence of AD in women is associated with the abrupt hormonal decline seen after menopause. However, other factors may be involved in this sex-related cognitive decline. Alterations in gut microbiota (GM) and its bioproducts have been reported in AD subjects and transgenic (Tg) mice, having a direct impact on brain amyloid-β pathology in male (M), but not in female (F) mice. Objective: The aim of this work was to determine GM composition and cognitive dysfunction in M and F wildtype (WT) and Tg mice, in a sex/genotype segregation design. Methods: Anxiety, short term working-memory, spatial learning, and long-term spatial memory were evaluated in 6-month-old WT and Tg male mice. Fecal short chain fatty acids were determined by chromatography, and DNA sequencing and bioinformatic analyses were used to determine GM differences. Results: We observed sex-dependent differences in cognitive skills in WT mice, favoring F mice. However, the cognitive advantage of females was lost in Tg mice. GM composition showed few sex-related differences in WT mice. Contrary, Tg-M mice presented a more severe dysbiosis than Tg-F mice. A decreased abundance of Ruminococcaceae was associated with cognitive deficits in Tg-F mice, while butyrate levels were positively associated with better working- and object recognition-memory in WT-F mice. Conclusion: This report describes a sex-dependent association between GM alterations and cognitive impairment in a mice model of AD.