4 research outputs found

    Mother-Infant Interactions: How Mothers of Hearing-Impaired Infants Interact With Their Babies Through Touch

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    Since the majority of their caregivers are hearing and use spoken language, most hearing-impaired infants (HII) are faced with a different language-learning problem than their age-matched hearing (AM) peers. A hearing mismatch occurs when a caregiver and her child receive variant levels of auditory input due to their different hearing abilities. Given that HII do not treat speech as a primary mode of communication, it is possible that their caregivers may exploit non-speech modalities when interacting with their infants—similar to deaf parents of deaf infants. However, due to mismatched hearing statuses, parents of HII may have a difficulty in utilizing the modality that best corresponds with their infants’ abilities. It is imperative to understand how hearing caregivers interact with their HII in order to explore the most relevant method of communication to enhance infants’ language learning. We video- and audio-recorded play interactions between mothers of HII (4 cochlear implant users; 2 hearing aid users) and mothers of AM peers (6 hearing). Mothers were given three toys and asked to play with their child, “as they would at home.” We measured pitch, duration, and intensity in their production of the names of the toys. We also measured the number and types of touches mothers produced. Results revealed that mothers of HII and AM peers had very similar measures for pitch, duration, and intensity. However, the number and type of touches were distinct: HII were touched more than three times more frequently than AM peers. Thus, findings from this study suggest that mothers of HII may exploit non-speech modalities when they have a hearing mismatch with their child

    New insights into the genetic etiology of Alzheimer’s disease and related dementias

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    Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

    New insights into the genetic etiology of Alzheimer’s disease and related dementias

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    Characterization of the genetic landscape of Alzheimer’s disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/‘proxy’ AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele
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