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Book Synopsis
In this book, the authors present current research in the study of the biological basis, management of symptoms and long-term neurological implications of cognitive dysfunction. Topics discussed in this compilation include the association of cognitive dysfunction with obstructive sleep apnea (OSA); chemotherapy-treated cancer patients who experience chemotherapy-related cognitive impairment during or after treatment sessions; alterations observed in glutamatergic/GABAergic circuitry in the brain in MS or CMS animal models that could be underlying in stress induced cognitive dysfunction; Coffin-Lowry syndrome as an X-linked intellectual disability caused by RSK2 protein kinase deficiency; bioeducational science as an emerging field to diagnose cognitive discomfort and specific learning disorders; and the systemic blockade of Cav2.1 mediated NMDA receptor signalling.

Cognitive Dysfunctions: Biological Basis,

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    A Hardback by Evan N Burgess, Luke A Thornton

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      Book details

      Publisher Nova Science Publishers Inc
      Published 1 December 2013
      ISBN-13 9781629484389
      978-1629484389
      ISBN-10 1629484385
      Also in:
      Science & Nature Neurosciences

      Description

      Book Synopsis
      In this book, the authors present current research in the study of the biological basis, management of symptoms and long-term neurological implications of cognitive dysfunction. Topics discussed in this compilation include the association of cognitive dysfunction with obstructive sleep apnea (OSA); chemotherapy-treated cancer patients who experience chemotherapy-related cognitive impairment during or after treatment sessions; alterations observed in glutamatergic/GABAergic circuitry in the brain in MS or CMS animal models that could be underlying in stress induced cognitive dysfunction; Coffin-Lowry syndrome as an X-linked intellectual disability caused by RSK2 protein kinase deficiency; bioeducational science as an emerging field to diagnose cognitive discomfort and specific learning disorders; and the systemic blockade of Cav2.1 mediated NMDA receptor signalling.

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