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Related Concept Videos

Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

54
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...
54
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

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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...
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Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

19
Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this...
19
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

35
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
35
Dementia l: Introduction01:22

Dementia l: Introduction

35
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
35

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Related Experiment Video

Updated: May 4, 2026

In Vitro Aggregation Assays Using Hyperphosphorylated Tau Protein
09:22

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Cerebral hypoperfusion reduces tau accumulation.

Ghupurjan Gheni1, Mitsuru Shinohara1,2, Masami Masuda-Suzukake3

  • 1Department of Aging Neurobiology, Center for Development of Advanced Medicine for Dementia, National Center for Geriatrics and Gerontology, 7-430 Morioka, Obu, Aichi, 474-8511, Japan.

Annals of Clinical and Translational Neurology
|December 2, 2024
PubMed
Summary

Cerebrovascular diseases like stroke may reduce Alzheimer's disease (AD) tau pathology. Chronic cerebral hypoperfusion lowers tau accumulation, potentially via enhanced microglial activity and cathepsin D, offering insights into multimorbidity.

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Area of Science:

  • Neuroscience
  • Neuropathology
  • Gerontology

Background:

  • Alzheimer's disease (AD) frequently co-occurs with cerebrovascular diseases.
  • The specific impact of cerebrovascular conditions on AD pathology is not well-defined.

Purpose of the Study:

  • To investigate the relationship between cerebrovascular diseases and Alzheimer's disease pathology.
  • To elucidate the mechanisms by which cerebral hypoperfusion influences tau accumulation.

Main Methods:

  • Analysis of clinical and neuropathological data from the National Alzheimer's Coordinating Center (NACC) database.
  • Utilized a mouse model with bilateral common carotid artery stenosis and tau seed injection to study chronic cerebral hypoperfusion's effects on tau pathology in neurons, astrocytes, microglia, and oligodendrocytes.

Main Results:

  • Clinical stroke history and lacunar infarcts correlated with reduced neurofibrillary tangle pathology in human data.
  • Cerebral hypoperfusion in the animal model decreased tau pathology across multiple cell types.
  • Activated astrocytes and microglia were observed under conditions of tau pathology and hypoperfusion.
  • Lysosomal enzyme cathepsin D levels increased with cerebral hypoperfusion.

Conclusions:

  • Cerebral hypoperfusion appears to reduce tau accumulation by increasing microglial phagocytosis of tau and enhancing degradation via cathepsin D.
  • Findings illuminate the interplay between tau pathology and cerebrovascular diseases in older adults with multiple health conditions.