Emotional Intelligence in Individuals With Intellectual disability

This chapter is aimed to draw attention to the integrated understanding of an individual with intellectual disability. It is very well known that intellectual disability is described as significant inefficiency in cognitive skills like learning, reasoning, problem solving, and in adaptive behavior, but this is not all when the individual is considered as a whole. This is where emotional intelligence comes in to help the individual cope with the cognitive disability. This chapter will discuss emotional intelligence in people with intellectual disability and how understanding of this will lead to better management plans for individual with intellectual disability, which will in turn lead to better empowerment. Further, this chapter will discuss the research gaps in this area and future study scope.

Herbal Approaches for Alzheimer Disease: A Review

"Plague of the Twenty-First Century," or “Alzheimer disease” is anneuro-degenerative disease that influenced the world's elderly population. The prevalence of Alzheimer's disease is expected to increase to one hundred thirty-five million by 2050, with no treatment(s) currently available to cure or monitor the disease's progression. The current treatment(s) have lesscapability to manage symptoms or delay disease development, and they can cause serious side effects. The cost of overall treatment is high for both the patients and their caregivers or family members. As an example, there is an serious requirement to find safer alternative treatments for better management of Alzheimer's disease. The various Indian herbal medicines such as Centella asiatica,Celastruspaniculatus Curcuma longa, Clitoriaternatea,Bacopa monnieri, Withania somnifera, has been reviewed in this article. Eclipta alba, Desmodiumgangeticum, Evolvulusalsinoides, Moringa oleifera, and Convolvulus pluricaulis are among the plants that have shown promising effect in the treatment related to cognitive disability.

Nanotechnology-Based Drug Delivery Strategies to Repair the Mitochondrial Function in Neuroinflammatory and Neurodegenerative Diseases

Mitochondria are vital organelles in eukaryotic cells that control diverse physiological processes related to energy production, calcium homeostasis, the generation of reactive oxygen species, and cell death. Several studies have demonstrated that structural and functional mitochondrial disturbances are involved in the development of different neuroinflammatory (NI) and neurodegenerative (ND) diseases (NI&NDDs) such as multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. Remarkably, counteracting mitochondrial impairment by genetic or pharmacologic treatment ameliorates neurodegeneration and clinical disability in animal models of these diseases. Therefore, the development of nanosystems enabling the sustained and selective delivery of mitochondria-targeted drugs is a novel and effective strategy to tackle NI&NDDs. In this review, we outline the impact of mitochondrial dysfunction associated with unbalanced mitochondrial dynamics, altered mitophagy, oxidative stress, energy deficit, and proteinopathies in NI&NDDs. In addition, we review different strategies for selective mitochondria-specific ligand targeting and discuss novel nanomaterials, nanozymes, and drug-loaded nanosystems developed to repair mitochondrial function and their therapeutic benefits protecting against oxidative stress, restoring cell energy production, preventing cell death, inhibiting protein aggregates, and improving motor and cognitive disability in cellular and animal models of different NI&NDDs.

Huntington disease update: new insights into the role of repeat instability in disease pathogenesis

The causative mutation for Huntington disease (HD), an expanded trinucleotide repeat sequence in the first exon of the huntingtin gene (HTT) is naturally polymorphic and inevitably associated with disease symptoms above 39 CAG repeats. Although symptomatic medical therapies for HD can improve the motor and non-motor symptoms for affected patients, these drugs do not stop the ongoing neurodegeneration and progression of the disease, which results in severe motor and cognitive disability and death. To date, there is still an urgent need for the development of effective disease‐modifying therapies to slow or even stop the progression of HD. The increasing ability to intervene directly at the roots of the disease, namely HTT transcription and translation of its mRNA, makes it necessary to understand the pathogenesis of HD as precisely as possible. In addition to the long-postulated toxicity of the polyglutamine-expanded mutant HTT protein, there is increasing evidence that the CAG repeat-containing RNA might also be directly involved in toxicity. Recent studies have identified cis- (DNA repair genes) and trans- (loss/duplication of CAA interruption) acting variants as major modifiers of age at onset (AO) and disease progression. More and more extensive data indicate that somatic instability functions as a driver for AO as well as disease progression and severity, not only in HD but also in other polyglutamine diseases. Thus, somatic expansions of repetitive DNA sequences may be essential to promote respective repeat lengths to reach a threshold leading to the overt neurodegenerative symptoms of trinucleotide diseases. These findings support somatic expansion as a potential therapeutic target in HD and related repeat expansion disorders.

Disability Associated with Chronic Graft-Versus-Host Disease after Allogeneic Hematopoietic Cell Transplantation

Chronic graft-versus-host disease (cGVHD) is the leading cause of late morbidity and mortality after allogeneic hematopoietic cell transplantation (HCT) and is associated with poor quality of life (QoL) and functional status among long-term HCT survivors. Disability is defined as any physical or mental impairment that limits a person's ability to do certain activities or interact with their environment. There are limited data regarding the association of cGVHD and disability. The aim of this study is to define disability and further understand contributing factors in patients with cGVHD. The Living With cGVHD Patient Survey was a cross-sectional online survey administered from May to August 2020 to US adult patients who reported a cGVHD diagnosis within the previous 5 years. Participants were recruited through patient advocacy groups and online patient panels. Respondents reported demographics, disease diagnosis, work status, cGVHD symptoms per Lee Symptom Scale (LSS), and impact on activities of daily living. Descriptive and correlational analyses were used to inform 3 composite definitions of disability: (1) severe cognitive disability (any report of severe limitation [>7 on a 0-10 scale] concerning managing personal finances, social interaction, or computer use); (2) severe physical disability (any report of severe limitation concerning personal hygiene; dressing; eating; or ability to use the restroom, move around the house, prepare meals, shop, do housework, or get around outside the home); and (3) work disability (any report of taking disability leave or leaving a job because of cGVHD). Out of 165 total survey respondents, 28 reported being retired, self-employed, or a homemaker and were excluded from the analysis as they were not considered part of the potentially employable general workforce (N=137). There were no demographic or cGVHD differences between respondents included in the study cohort vs those who were excluded. Nearly half of respondents (47%) reported severe cognitive limitations in at least 1 of the activities of the composite score (Figure 1). Univariable analyses demonstrated that cGVHD severity/duration (P=0.0056); LSS eye (P=0.0266), mouth (P=0.0132), lung (P=0.0002), skin, nutrition, energy, and psychological symptoms (P<0.0001 for all); and number of treatments (P=0.0210) and specialists seen (P=0.0030) were all associated with self-reported severe cognitive disability. Skin and psychological symptoms and number of specialists seen remained significant in a multivariable analysis (Table 1). Two-thirds (67%) of respondents reported severe physical disability associated with cGVHD (Figure 1). In univariable analyses, cGVHD severity/duration (P=0.0003); LSS skin (P=0.0112), eyes (P=0.0107), psychological (P=0.0003), mouth, lungs, nutrition, energy symptoms (P<0.0001 for all); and number of treatments (P=0.0323) and specialists seen (P=0.0275) were associated with physical disability. In a multivariable analysis, female sex and energy, mouth, and nutrition symptoms were found to be significant (Table 1). Nearly two-thirds of respondents (63%) reported work disability (Figure 1). In univariable analyses, non-White race (P=0.0248); cGVHD severity/duration (P=0.0220); LSS skin (P=0.005), eyes (P=0.0239), mouth (P=0.0222), lungs (P=0.0011), nutrition (P=0.0010), energy (P<0.0001), and psychological symptoms (P=0.0014); and number of specialists seen (P=0.0495) were associated with work disability. Results from a multivariable analysis confirmed race and energy to be factors significantly associated with work disability (Table 1). A substantial proportion of survey respondents reported severe cognitive and physical disability, as well as work-related disability, associated with cGVHD, highlighting the importance of defining and better understanding cGVHD-associated disability. Additional investigations of the impact of work type, sex and racial disparities, and specific cGVHD symptoms are needed to further understand this relationship and improve the overall health-related QoL of long-term HCT survivors. Figure 1 Figure 1. Disclosures Hamilton: Syndax: Membership on an entity's Board of Directors or advisory committees; Equilium: Membership on an entity's Board of Directors or advisory committees. Williams: Incyte Corporation: Other: Employee of IQVIA, the company commissioned by Incyte Corporation to conduct this study. Flore: Incyte Corporation: Other: Employee of IQVIA, the company commissioned by Incyte Corporation to conduct this study. Galvin: Incyte Corporation: Current Employment, Current equity holder in publicly-traded company. Turnbull: Incyte Corporation: Other: Employee of IQVIA, the company commissioned by Incyte Corporation to conduct this study. Yu: Incyte Corporation: Current Employment, Current holder of individual stocks in a privately-held company.

Erinacine A-Enriched Hericium erinaceus Mycelium Delays Progression of Age-Related Cognitive Decline in Senescence Accelerated Mouse Prone 8 (SAMP8) Mice

There have been many reports on the neuroprotective effects of Hericium erinaceus mycelium, in which the most well-known active compounds found are diterpenoids, such as erinacine A. Previously, erinacine A-enriched Hericeum erinaceus mycelium (EAHEM) was shown to decrease amyloid plaque aggregation and improve cognitive disability in Alzheimer’s disease model APP/PS1 mice. However, its effects on brain aging have not yet been touched upon. Here, we used senescence accelerated mouse prone 8 (SAMP8) mice as a model to elucidate the mechanism by which EAHEM delays the aging of the brain. Three-month-old SAMP8 mice were divided into three EAHEM dosage groups, administered at 108, 215 and 431 mg/kg/BW/day, respectively. During the 12th week of EAHEM feeding, learning and memory of the mice were evaluated by single-trial passive avoidance and active avoidance test. After sacrifice, the amyloid plaques, induced nitric oxidase synthase (iNOS) activity, thiobarbituric acid-reactive substances (TBARS) and 8-OHdG levels were analyzed. We found that the lowest dose of 108 mg/kg/BW EAHEM was sufficient to significantly improve learning and memory in the passive and active avoidance tests. In all three EAHEM dose groups, iNOS, TBARS and 8-OHdG levels all decreased significantly and showed a dose-dependent response. The results indicate that EAHEM improved learning and memory and delayed degenerative aging in mice brains.