Vectorized nanodelivery systems for ischemic stroke: a concept and a need

Abstract

Neurological diseases of diverse aetiologies have significant effects on the quality of life of patients. The limited self-repairing capacity of the brain is considered to be the origin of the irreversible and progressive nature of many neurological diseases. Therefore, neuroprotection is an important goal shared by many clinical neurologists and neuroscientists. In this review, we discuss the main obstacles that have prevented the implementation of experimental neuroprotective strategies in humans and propose alternative avenues for the use of neuroprotection as a feasible therapeutic approach. Special attention is devoted to nanotechnology, which is a new approach for developing highly specific and localized biomedical solutions for the study of the multiple mechanisms involved in stroke. Nanotechnology is contributing to personalized neuroprotection by allowing us to identify mechanisms, determine optimal therapeutic windows, and protect patients from brain damage. In summary, multiple aspects of these new players in biomedicine should be considered in future in vivo and in vitro studies with the aim of improving their applicability to clinical studies.

CU06-1004 (endothelial dysfunction blocker) ameliorates astrocyte end-feet swelling by stabilizing endothelial cell junctions in cerebral ischemia/reperfusion injury

“…Reperfusion can be achieved either through thrombolysis using thrombolytic reagents or the surgical removal of thrombi [2]. Despite known beneficial effects, reperfusion causes detrimental effects, including edema, blood-brain barrier (BBB) breakdown, and astrocyte endfeet swelling in stroke patients [2][3][4]. However, the underlying mechanisms associated with reperfusion damage remain poorly understood.…”

Molecular and Pharmacological Modulation of CALHM1 Promote Neuroprotection against Oxygen and Glucose Deprivation in a Model of Hippocampal Slices

“…Those pathological conditions induce overactivation of astrocytes and microglia. These two cell types in brain parenchyma under pathological situations lead to an increase in the production and release of ROS and inflammatory mediators, worsening neuronal damage [25]. Once demonstrated that CALHM1 ablation has a neuroprotective profile, we decided to go further by measuring ROS production in hippocampal slices from each experimental group.…”

Recent Advances in the Therapeutic and Diagnostic Use of Liposomes and Carbon Nanomaterials in Ischemic Stroke

“…The increase in intracellular Ca 2+ concentration initiates a series of cytoplasmic and nuclear events that result in cellular damage, such as the production of ROS. ROS accumulation, particularly after reperfusion, will cause mitochondrial ( Da Silva-Candal et al, 2017 ) and cellular membrane damage ( Dugan and Choi, 1994 ). Intracellular signaling pathways triggered during excitotoxicity also stimulate the production of pro-inflammatory mediators ( Dirnagl et al, 1999 ).…”

“…Moreover, the complexity of the physiopathological events that take place during cerebral ischemia and the still limited knowledge about the molecular and cellular mechanisms involved and their spatial and temporal occurrence represent an obstacle to the identification of effective tissue biomarkers and the design of powerful nanotechnology-based strategies for diagnosis and therapy ( Da Silva-Candal et al, 2017 ).…”