Making Meaning Together:Embodied Narratives in a Case of Severe Autism

Shared understanding is generated between individuals before speech through a language of body movement and non-verbal vocalisation, expression of feeling and interest made in gestures of movement and voice. Human understanding is co-created in these embodied projects, displayed in serially organised expressions with shared timing of reciprocal actions between partners. These develop in narrative events that build over cycles of reciprocal expressive action in a four-part structure shared by all the time-based arts: ‘introduction’, ‘development’, ‘climax’, and ‘conclusion’. Pre-linguistic narrative establishes the foundation of later, linguistic intelligence. Yet, participating in social interactions that give rise to narrative development is a central problem of autism spectrum disorder. In this paper, we examine the rapid growth of narrative meaning-making between a non-verbal young woman with severe autism and her new therapist. Episodes of embodied, shared understanding were enabled through a basic therapeutic mode of reciprocal, creative mirroring of expressive gesture. These developed through reciprocal cycles and as the relationship progressed, complete co-created narratives were formed resulting in shared joy and the mutual interest and trust of companionship. These small, embodied stories enabled moments of co-regulated arousal that the young woman had previous difficulty with. These data provide evidence for an intact capacity for non-verbal narrative meaning-making in autism

Making meaning together : embodied narratives in a case of severe autism

Human narrative understanding is co-created in imaginative projects and experiences displayed in serially organised expressions of gesture and voice. Shared timing of reciprocal actions develop between two or more persons in narrative events that build over cycles in a four-part structure of 'introduction', 'development', 'climax', and 'conclusion'. Pre-linguistic narrative establishes the foundation of later, linguistic intelligence. Yet, participating in social interactions that give rise to narrative development is a central problem of autism spectrum disorder. In this paper, we examine the rapid growth of narrative meaning-making between a non-verbal young woman with severe autism and her new therapist. Episodes of embodied, shared understanding were enabled through a basic therapeutic mode of reciprocal, creative mirroring of expressive gesture. These developed through reciprocal cycles and as the relationship progressed, complete co-created narratives were formed resulting in shared joy and the mutual interest and trust of companionship. These small, embodied stories enabled moments of co-regulated arousal that the young woman had previous difficulty with. These data provide evidence for an intact capacity for non-verbal narrative meaning-making in autism

Limitations of the human iPSC-derived neuron model for early-onset Alzheimers disease.

Non-familial Alzheimers disease (AD) occurring before 65 years of age is commonly referred to as early-onset Alzheimers disease (EOAD) and constitutes ~ 5-6% of all AD cases (Mendez et al. in Continuum 25:34-51, 2019). While EOAD exhibits the same clinicopathological changes such as amyloid plaques, neurofibrillary tangles (NFTs), brain atrophy, and cognitive decline (Sirkis et al. in Mol Psychiatry 27:2674-88, 2022; Caldwell et al. in Mol Brain 15:83, 2022) as observed in the more prevalent late-onset AD (LOAD), EOAD patients tend to have more severe cognitive deficits, including visuospatial, language, and executive dysfunction (Sirkis et al. in Mol Psychiatry 27:2674-88, 2022). Patient-derived induced pluripotent stem cells (iPSCs) have been used to model and study penetrative, familial AD (FAD) mutations in APP, PSEN1, and PSEN2 (Valdes et al. in Research Square 1-30, 2022; Caldwell et al. in Sci Adv 6:1-16, 2020) but have been seldom used for sporadic forms of AD that display more heterogeneous disease mechanisms. In this study, we sought to characterize iPSC-derived neurons from EOAD patients via RNA sequencing. A modest difference in expression profiles between EOAD patients and non-demented control (NDC) subjects resulted in a limited number of differentially expressed genes (DEGs). Based on this analysis, we provide evidence that iPSC-derived neuron model systems, likely due to the loss of EOAD-associated epigenetic signatures arising from iPSC reprogramming, may not be ideal models for studying sporadic AD

Limitations of the human iPSC-derived neuron model for early-onset Alzheimer’s disease

Abstract Non-familial Alzheimer’s disease (AD) occurring before 65 years of age is commonly referred to as early-onset Alzheimer’s disease (EOAD) and constitutes ~ 5–6% of all AD cases (Mendez et al. in Continuum 25:34–51, 2019). While EOAD exhibits the same clinicopathological changes such as amyloid plaques, neurofibrillary tangles (NFTs), brain atrophy, and cognitive decline (Sirkis et al. in Mol Psychiatry 27:2674–88, 2022; Caldwell et al. in Mol Brain 15:83, 2022) as observed in the more prevalent late-onset AD (LOAD), EOAD patients tend to have more severe cognitive deficits, including visuospatial, language, and executive dysfunction (Sirkis et al. in Mol Psychiatry 27:2674–88, 2022). Patient-derived induced pluripotent stem cells (iPSCs) have been used to model and study penetrative, familial AD (FAD) mutations in APP, PSEN1, and PSEN2 (Valdes et al. in Research Square 1–30, 2022; Caldwell et al. in Sci Adv 6:1–16, 2020) but have been seldom used for sporadic forms of AD that display more heterogeneous disease mechanisms. In this study, we sought to characterize iPSC-derived neurons from EOAD patients via RNA sequencing. A modest difference in expression profiles between EOAD patients and non-demented control (NDC) subjects resulted in a limited number of differentially expressed genes (DEGs). Based on this analysis, we provide evidence that iPSC-derived neuron model systems, likely due to the loss of EOAD-associated epigenetic signatures arising from iPSC reprogramming, may not be ideal models for studying sporadic AD