Injury Mechanisms in Stroke

The occurrence of stroke induces a series of complex responses, which in turn leads to a set of complex pathological changes, and different types of stroke cause different cascades of responses. Although research related to the injury mechanisms of stroke has been conducted for decades, many mysteries remain unanswered. To accelerate the understanding of stroke, Ace Neuroscience  offers a comprehensive service to explore the pathogenic mechanisms of stroke injury.

Injury Mechanism in Ischemic Stroke

Ischemic stroke is the most common form of stroke. The center of the brain region with reduced blood flow after ischemia is the ischemic core, and within this region, neurons undergo irreversible death within minutes. Surrounding the ischemic core is the penumbra, an area that keeps neurons quiescent because of a collateral blood supply. If blood flow to the penumbra is not restored, these neurons remain dead eventually and become part of the ischemic infarct. Ischemic stroke activates a series of harmful signaling cascades, including excitotoxicity, oxidative stress, neuroinflammation, and blood-brain barrier breakdown, which ultimately lead to neuronal death.

Schematic representation of ischemia induced signaling cascade in the brainFig. 1 Schematic representation of ischemia induced signaling cascade in the brain (Paul, et al., 2021)

Injury Mechanism in Hemorrhagic Stroke

The occurrence of a hemorrhagic stroke induces a cascade leading to primary and secondary brain injury.

  • Primary brain injury is caused by mass effect and mechanical disruption from extravasated blood. When extravasated blood enters the brain parenchyma or/and subarachnoid space, there is an immediate increase in intracranial pressure and mechanical compression of local structures. The increase in intracranial pressure leads to arterial compression and ischemia.
  • Secondary brain injury is caused by the toxic biochemical and metabolic effects of extravasated blood components in response to the physiological response to the hematoma (mainly edema and inflammation). Perihematomal edema, intravascular edema, and global edema that occur after ICH and SAH are related to poor clinical outcomes and may lead to more severe secondary injury. Blood components, such as thrombin, hemoglobin, and its degradation products, can lead to cerebral edema through blood brain barrier (BBB) destruction and toxic effects. At the same time, neuroinflammation after hemorrhagic stroke is responsible for triggering vasogenic edema through BBB destruction and cellular edema through toxic effects on cells. Ischemic injury, self-regulatory dysfunction, and thrombus retraction are also related to brain edema after a hemorrhagic stroke.

Schematic representation of hemorrhagic induced signaling cascade in the brainFig. 2 Schematic representation of hemorrhagic induced signaling cascade in the brain

Ace Neuroscience is a biological company specializing in pre-clinical CRO services for stroke. We have professional scientists, the latest technology, and advanced equipment. Our company provides stroke-related services such as basic research and stroke therapy development. We work with you to gain insight into the pathogenesis of stroke and develop more effective treatments. Feel free to contact us with any stroke-related questions.

References
  1. Xu, Y., et al., Nanomedicine: An emerging novel therapeutic strategy for hemorrhagic stroke. Int J Nanomedicine, 2022. 17: p. 1927-1950.
  2. Paul, S.Candelario-Jalil, E., Emerging neuroprotective strategies for the treatment of ischemic stroke: An overview of clinical and preclinical studies. Exp Neurol, 2021. 335: p. 113518.
All of our services are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
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