Publications by authors named "C E DeJesus"

Objective: Gain-of-function variants in the KCNT1 gene, which encodes a sodium-activated potassium ion channel, drive severe early onset developmental epileptic encephalopathies including epilepsy of infancy with migrating focal seizures and sleep-related hypermotor epilepsy. No therapy provides more than sporadic or incremental improvement. Here, we report suppression of seizures in a genetic mouse model of KCNT1 epilepsy by reducing Kcnt1 transcript with divalent small interfering RNA (siRNA), an emerging variant of oligonucleotide technology developed for the central nervous system.

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Introduction: Positionality statements accompanying peer-reviewed publications are increasingly being implemented in academic journals across many disciplines, including psychology. These statements serve as transparent, public acknowledgments of the authors' identities, which can offer valuable insight into the authors' work in the context of their lived experiences and potential biases. However, journal editors and associated staff risk harm by uniformly adopting a policy on positionality statements without consideration of the unintended consequences of implementing such practices.

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Objective: Consistent data support an association between anxiety and eating disorders (EDs), and theoretical models of EDs suggest that anxiety may be involved in the etiology and maintenance of ED symptoms over time. However, the directionality of relations between these variables remains under-characterized, particularly within treatment settings.

Method: We used bivariate latent change score models to explore longitudinal associations between anxiety and ED symptoms in a sample of ED patients (N = 548, 93.

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Objective: Written exposure therapy (WET) is a brief treatment for posttraumatic stress disorder (PTSD), with an increasing number of studies published over the past several years. The current study conducted a systematic review to evaluate the current state of evidence for WET as a treatment for PTSD symptom severity.

Method: Four databases were searched: PsycInfo, PTSDpubs, MEDLINE, and PubMed.

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Neuroinflammation is a key driver of neurodegenerative disease, however the tools available to model this disease biology at the systems level are lacking. We describe a translational drug discovery platform based on organotypic culture of murine cortical brain slices that recapitulate disease-relevant neuroinflammatory biology. After an acute injury response, the brain slices assume a chronic neuroinflammatory state marked by transcriptomic profiles indicative of activation of microglia and astrocytes and loss of neuronal function.

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