Topic: social deficits

Progressive impairment of cognition is a key clinical feature of Alzheimer’s disease (AD), characterized by the accumulation of amyloid beta-protein (Aβ), tau hyperphosphorylation, neuroinflammation, and neuronal degeneration.Cannabidiol (CBD) is a safe, non-psychoactive phytocannabinoid that exhibits immunomodulatory activity in neurodegenerative disease, may ameliorate AD symptoms and slow cognitive decline.In this study, we aimed to examine whether chronic treatment with CBD can prevent cognitive and social deficits in a rat model of sporadic AD, and whether these changes are associated wit

Autism Spectrum Disorder (ASD) is characterized by impairments in social communication and interactions, as well as restricted behaviours. Strikingly most of ASD patients also exhibit aberrant reactivity to sensory stimuli including tactile stimuli. Tactile information is perceived in the periphery and processed in the spinal cord under the control of inhibitory neurons before being sent to higher brain structures. However, whether these inhibitory neurons undergo functional alterations in ASD models remains poorly investigated. To explore the functional plasticity of those neurons in ASD, we

Cognitive and social deficits are core to most psychiatric diseases. Dysfunctional connectivity in brain networks, including the prefrontal cortex (PFC) and its interacting subcortical structures, is supposed to elicit these deficits. Stress exposure and the ensuing release of glucocorticoid hormones is a common risk factor for psychiatric diseases and is known to modulate cognitive function partly through its binding to its receptor GR. The general aim of this work is to study the impact of stress exposure on PFC function and its extended brain networks. As expected, we show here that repeate

Hippocampal subregion CA2 has been implicated in social memory. CA2 contains spatially modulated “place cells” that change their firing patterns (“remap”) during social interactions (Alexander et al., 2016). Our preliminary results suggest that CA2 place cell remapping is driven by the olfactory content of social experiences. Fragile X Syndrome (FXS) is a neurodevelopmental disorder associated with abnormal social behaviors. To our knowledge, the activity of CA2 place cells during social interactions has not been examined in relation to FXS. Here, we recorded CA2 place cells in wildtype (WT) c

Migraine, a neurological disorder characterized by recurring, intense headaches, disproportionately affects a significant portion of the population, particularly females. While its precise etiology remains elusive, it is thought to have arisen from a combination of genetic predisposition and environmental factors. This research endeavors to explore the neurobiological underpinnings of both the sensory and emotional aspects of migraine pain, as well as the associated social impairments. Using the nitroglycerin (NTG) migraine model, which induces vasodilation via systemic administration, we simu

Social deficits play a role in numerous psychiatric, neurological and neurodevelopmental disorders. Relating complex behavior, such as social interaction, to brain activity remains one of the biggest goals and challenges in neuroscience. Availability of standardized behavioral tests that assess social preference is however, limited. Here, we present a novel behavioral set-up and paradigm that we developed to measure social behavior, the modified elevated gap interaction test (MEGIT). In this test, animals are placed on one of two elevated platforms separated by a gap, in which they can engage

Diverse neurodevelopmental syndromes (e.g. Fragile X) are caused by alterations in specific genes leading to pervasive impairments comorbid with autism (i.e. social and repetitive behaviors). Although all ASDs converge into common core behaviors, genetic variants in ASD are very heterogeneous. Here, we describe a cleavable cell adhesion molecule (Negr1) as upregulated in the brain of 5 diverse mouse models of ASDs (including Fragile X) and postmortem brains from people with autism or Fragile X, and causative of core ASD behaviors and brain alterations when up-regulated in wild-type (WT) animal