Plasma β-amyloid levels in cerebral amyloid angiopathy-associated hemorrhagic stroke

Mar Hernandez-Guillamon1, Pilar Delgado, Anna Penalba

  • 1Neurovascular Research Laboratory, Institut de Recerca, Universitat Autònoma de Barcelona, Barcelona, Spain.

Insights

Specific beta-amyloid (Aβ) fragments in plasma, including Aβ(1-42) and Aβ(N-42), show elevated levels in patients with cerebral amyloid angiopathy (CAA). These findings suggest potential for plasma Aβ as a diagnostic biomarker for CAA.

Area of Science:

  • Neurology
  • Biochemistry
  • Geriatrics

Background:

  • Cerebral amyloid angiopathy (CAA) is a primary cause of intracerebral hemorrhage (ICH) in elderly individuals.
  • Early and accurate diagnosis of CAA is crucial for managing neurological conditions.

Purpose of the Study:

  • To identify plasma beta-amyloid (Aβ) species as potential biomarkers for diagnosing cerebral amyloid angiopathy (CAA).
  • To differentiate between CAA subtypes and disease severity using plasma Aβ profiles.

Main Methods:

  • Quantified plasma levels of Aβ(1-40), Aβ(N-40), Aβ(1-42), and Aβ(N-42) using xMAP® technology.
  • Utilized CT scans and brain MRI for hemorrhage identification and classification.
  • Assessed patients using the Boston criteria for probable or possible CAA.

Main Results:

  • Elevated plasma levels of full-length Aβ(1-42) and truncated Aβ(N-42) were observed in probable CAA patients compared to controls.
  • Full-length Aβ(1-40) was significantly higher in probable CAA cases versus possible CAA and controls.
  • Increased plasma Aβ(N-42) correlated with the presence of multiple lobar macrohemorrhages, indicating a link to CAA severity.

Conclusions:

  • Specific plasma Aβ fragments, particularly Aβ(1-42) and Aβ(N-42), show promise as diagnostic biomarkers for cerebral amyloid angiopathy (CAA).
  • These Aβ species may aid in the early detection and characterization of CAA, improving patient management.
Abstract

Related Concept Videos

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...
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...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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 barrier loses...
Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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 microglia. Abnormal...