Astrocytic Abnormalities in Schizophrenia

Astrocytes are glial cells in the central nervous system (CNS), which contribute to CNS health and disease by participating in homeostatic, structural, and metabolic processes that play an essential role in facilitating synaptic transmission between neurons. Schizophrenia (SCZ) is a neuropsychiatric disorder associated with various positive and negative behaviors and interruption of executive function and cognition thought to be due partly to aberrations in signaling within neural networks. Recent research has demonstrated that astrocytes play a role in SCZ through various effects, including influencing immune system function, altering white matter, and mediating changes in neurotransmitters. Astrocytes are also known to play a role in inducing SCZ-associated changes in neuroplasticity, which includes alterations in synaptic strength and neurogenesis. Also, astrocyte abnormalities are linked to neurobehavioral impairments seen at the clinical level. The present chapter details general information on SCZ. It highlights the role of astrocytes in SCZ at molecular and behavioral levels, including neural changes seen in the disease, and the therapeutic implications of targeting astrocytes in SCZ

Lupus and the Nervous System: A Neuroimmunoloigcal Update on Pathogenesis and Management of Systemic Lupus Erythematosus with Focus on Neuropsychiatric SLE

An autoimmune condition is characterized by a misdirected immunological system that interacts with host antigens. Excess activation of T- and B-lymphocytes, autoantibody generation, immune complex deposition, and multi-organ injury are found in systemic lupus erythematosus (SLE), an early autoimmune condition with a substantial hereditary element. A number of environmental factors and lifestyle changes also play a role in the development of SLE. The imbalanced immunity could take part in the dysfunction and injury of different biological organs, including the central and peripheral nervous systems. Neuropsychiatric SLE (NPSLE) can present with focal and diffuse involvements. Clinical manifestations of NPSLE vary from mild cognitive deficits to changed mental status, psychosis, and seizure disorders. Headaches, mood, and cognitive problems are the most common neuropsychiatric presentations associated with SLE. NPSLE could be found in 40% of all people who have SLE. The diagnostic inference of NPSLE can be made solely following these secondary causes have been ruled out. The present chapter provides an updated discussion of the clinical presentation, molecular processes, diagnosis, management, and therapy of SLE with emphasizing on NPSLE

Deep brain stimulation (DBS) as a therapeutic approach in gait disorders: What does it bring to the table?

Gait deficits are found in various degenerative central nervous system conditions, and are particularly a hallmark of Parkinson’s disease (PD). While there is no cure for such neurodegenerative disorders, Levodopa is considered as the standard medication in PD patients. Often times, the therapy of severe PD consists of deep brain stimulation (DBS) of the subthalamic nucleus. Earlier research exploring the effect of gait have reported contradictory results or insufficient efficacy. A change in gait includes various parameters, such as step length, cadence, Double-stance phase duration which may be positively affected by DBS. DBS could also be effective in correcting the levodopa-induced postural sway abnormalities. Moreover, during normal walking, interaction among the subthalamic nucleus and cortex —essential regions which exert a role in locomotion— are coupled. However, during the freezing of gait, the activity is desynchronized. The mechanisms underlying DBS-induced neurobehavioral improvements in such scenarios requires further study. The present review discusses DBS in the context of gait, the benefits associated with DBS compared to standard pharmacotherapy options, and provides insights into future research