Compromised neuromuscular function of walking in people with diabetes: A narrative review.

AIM: This review summarizes recent studies that have investigated the neuromuscular dysfunction of walking in people with diabetes and its relationship to ulcer formation. METHODS: A comprehensive electronic search in the database (Scopus, Web of Science, PsycINFO, ProQuest, and PubMed) was performed for articles pertaining to diabetes and gait biomechanics. RESULTS: The Achilles tendon is thicker and stiffer in those with diabetes. People with diabetes demonstrate changes in walking kinematics and kinetics, including slower self-selected gait speed, shorter stride length, longer stance phase duration, and decreased ankle, knee, and metatarsophalangeal (MTP) joint range of motion. EMG is altered during walking and may reflect diabetes-induced changes in muscle synergies. Synergies are notable because they provide a more holistic pattern of muscle activations and can help develop better tools for characterizing disease progression. CONCLUSION: Diabetes compromises neuromuscular coordination and function. The mechanisms contributing to ulcer formation are incompletely understood. Diabetes-related gait impairments may be a significant independent risk factor for the development of foot ulcers.

Zika virus infects pericytes in the choroid plexus and enters the central nervous system through the blood-cerebrospinal fluid barrier.

Zika virus (ZIKV) can infect and cause microcephaly and Zika-associated neurological complications in the developing fetal and adult brains. In terms of pathogenesis, a critical question is how ZIKV overcomes the barriers separating the brain from the circulation and gains access to the central nervous system (CNS). Despite the importance of ZIKV pathogenesis, the route ZIKV utilizes to cross CNS barriers remains unclear. Here we show that in mouse models, ZIKV-infected cells initially appeared in the periventricular regions of the brain, including the choroid plexus and the meninges, prior to infection of the cortex. The appearance of ZIKV in cerebrospinal fluid (CSF) preceded infection of the brain parenchyma. Further the brain infection was significantly attenuated by neutralization of the virus in the CSF, indicating that ZIKV in the CSF at the early stage of infection might be responsible for establishing a lethal infection of the brain. We show that cells infected by ZIKV in the choroid plexus were pericytes. Using in vitro systems, we highlight the possibility that ZIKV crosses the blood-CSF barrier by disrupting the choroid plexus epithelial layer. Taken together, our results suggest that ZIKV might exploit the blood-CSF barrier rather than the blood-brain barrier to invade the CNS.