Social deficits, such as poor social skills (i.e., the inability to engage in appropriate and effective social interactions) and social withdrawal, are prevalent across psychiatric disorders and often co-occur with hippocampal structural and functional abnormalities. The centrality of both social and hippocampal dysfunction in psychiatric research prompts the question: Are they linked? The social cognitive map framework provides a clue: The hippocampus tracks social information in the physical environment, maps others along social dimensions, and supports social memory and decision-making. Hippocampal dysfunction might disrupt social map representation and contribute to commonly seen social behavioral symptoms. This review summarizes evidence for the role of the hippocampus in social cognitive mapping, followed by evidence that hippocampal dysfunction and social dysfunction co-occur in psychiatric disorders. We argue that the co-occurrence of hippocampal and social impairment may be related via hippocampal social cognitive mapping.
Alzheimer's disease (AD) is a neurodegenerative disorder that results in significant memory impairment and cognitive decline. Current medical treatment is aimed at treating AD symptoms but does not alter the disease course. The use of deep brain stimulation (DBS) for the treatment of AD is in its nascent phase. Here, we describe the evolution of DBS as a potential treatment modality for AD, including previous and current trials, as well as the behavioral and histological preclinical data that help to better understand and inform future clinical trials. As such, a phase 3 clinical trial studying the effects of forniceal DBS for AD is currently underway.
Sleep is important for cognitive ability, and perturbations of sleep are associated with a myriad of brain disorders. However, how sleep promotes health and function during wake is poorly understood. To address the cellular and molecular mechanisms underlying sleep, we use the fruit fly Drosophila melanogaster as a genetic model. Forward genetic approaches in flies were critical for deciphering molecular mechanisms of the circadian clock. Using similar approaches, we and others are gaining insights into the pathways that control sleep amount.
The advent of the noninvasive brain stimulation (NIBS) technique has paved the way for neural circuit-based treatments for addiction. Recently, evidence from both preclinical and clinical studies has evaluated the use of transcranial magnetic stimulation (TMS) as a safe and cost-effective therapeutic tool for substance use disorders (SUDs). Indeed, repetitive TMS impacts on neural activity inducing short- and long-term effects involving neuroplasticity mechanisms locally within the target area of stimulation and the network level throughout the brain. Here, we provide an integrated view of evidence highlighting the mechanisms of TMS-induced effects on modulating the maladaptive brain circuitry of addiction. We then review the preclinical and clinical findings suggesting rTMS as an effective interventional tool for the treatment of SUDs.