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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
Stroke: Introduction and Types01:29

Stroke: Introduction and Types

A stroke is an acute neurological event caused by the sudden disruption of cerebral blood flow, leading to rapid loss of neuronal function. Neurons depend on continuous oxygen and glucose supply, so even brief interruptions can cause irreversible injury within minutes. Strokes are classified into ischemic and hemorrhagic types.Ischemic StrokeIschemic strokes are most common and occur due to arterial occlusion, depriving brain tissue of oxygen and nutrients. This leads to energy failure, ionic...

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Related Experiment Video

Updated: Jul 7, 2026

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke
05:40

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

Published on: November 29, 2024

Akt1 gene deletion and stroke.

Jun Li1, Jesse Lang, Zhiyuan Zeng

  • 1Department of Neurology, University of Connecticut Health Center, Farmington CT, 06030, United States.

Journal of the Neurological Sciences
|February 9, 2008
PubMed
Summary

The Akt protein

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Akt activation is crucial for neuronal survival post-ischemic injury.
  • Estrogen is known to enhance Akt activity, but its role in male vs. female brains is unclear.
  • Akt is a potential target for neuroprotection after stroke.

Purpose of the Study:

  • To investigate the role of Akt isoforms in stroke outcome.
  • To determine if estrogen's neuroprotective effects are mediated by Akt.
  • To evaluate the efficacy of Akt inhibition in a stroke model.

Main Methods:

  • Utilized a focal stroke model in mice.
  • Employed genetic deletion of the Akt1 isoform.
  • Administered pharmacological Akt inhibition using triciribine.

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Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
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Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

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Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique
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Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique

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Last Updated: Jul 7, 2026

AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke
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AAV Systems and Mouse Models for Investigating Ectopic Expression of Neurod1 in Transduced Cells at Subacute and Chronic Times Post-Ischemic Stroke

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Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
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Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

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Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique
07:34

Induction of Acute Ischemic Stroke in Mice Using the Distal Middle Artery Occlusion Technique

Published on: December 15, 2023

  • Assessed stroke outcome and levels of phosphorylated Akt (p-Akt).

    • Main Results:

    • Akt1 deletion did not alter stroke outcome in male or female mice.
    • Alternative Akt isoforms compensated for Akt1 loss, maintaining p-Akt levels.
    • Estrogen's neuroprotective effects persisted in Akt1-deficient mice without increasing p-Akt.
    • Pan-Akt inhibition with triciribine did not affect stroke outcome despite reduced p-Akt.

    Conclusions:

    • Akt1 is not essential for stroke outcome, as other isoforms can compensate.
    • Estrogen's neuroprotective mechanisms may not solely rely on Akt activation.
    • The role of Akt in ischemic stroke outcome remains uncertain.
    • Limitations exist in using genetic models to study Akt's function in stroke.