X-ray fluorescence mapping of brain tissue reveals the profound extent of trace element dysregulation in stroke pathophysiology.

The brain is a privileged organ with regard to its trace element composition and maintains a robust barrier system to sequester this specialized environment from the rest of the body and the vascular system. Stroke is caused by loss of adequate blood flow to a region of the brain. Without adequate blood flow ischaemic changes begin almost immediately, triggering an ischaemic cascade, characterized by ion dysregulation, loss of function, oxidative damage, cellular degradation, and breakdown of the barrier that helps maintain this environment.

Ion Dyshomeostasis in the Early Hyperacute Phase after a Temporary Large-Vessel Occlusion Stroke.

Element dysregulation is a pathophysiologic hallmark of ischemic stroke. Prior characterization of post-stroke element dysregulation in the photothrombotic model demonstrated significant element changes for ions that are essential for the function of the neurovascular unit. To characterize the dynamic changes during the early hyperacute phase (<6 h), we employed a temporary large-vessel occlusion stroke model.

Investigating Cu(I) binding to model peptides of N-terminal Aβ isoforms.

Amyloid beta (Aβ) peptides and copper (Cu) ions are each involved in critical biological processes including antimicrobial activity, regulation of synaptic function, angiogenesis, and others. Aβ binds to Cu and may play a role in Cu trafficking. Aβ peptides exist in isoforms that vary at their C-and N-termini; variation at the N-terminal sequence affects Cu binding affinity, structure, and redox activity by providing different sets of coordinating groups to the metal ion.

A review of concepts and methods for FTIR imaging of biomarker changes in the post-stroke brain.

Stroke represents a core area of study in neurosciences and public health due to its global contribution toward mortality and disability. The intricate pathophysiology of stroke, including ischemic and hemorrhagic events, involves the interruption in oxygen and nutrient delivery to the brain. Disruption of these crucial processes in the central nervous system leads to metabolic dysregulation and cell death.

Neuronal and Astrocyte Insulin-like Growth Factor-1 Signaling Differentially Modulates Ischemic Stroke Damage.

Ischemic stroke is a leading cause of death and disability, as therapeutic options for mitigating the long-term deficits precipitated by the event remain limited. Acute administration of the neuroendocrine modulator insulin-like growth factor-1 (IGF-1) attenuates ischemic stroke damage in preclinical models, and clinical studies suggest IGF-1 can reduce the risk of stroke and improve overall outcomes. The cellular mechanism by which IGF-1 exerts this protection is poorly defined, as all cells within the neurovascular unit express the IGF-1 receptor.