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Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry
09:31

Visualization of Amyloid β Deposits in the Human Brain with Matrix-assisted Laser Desorption/Ionization Imaging Mass Spectrometry

Published on: March 7, 2019

MR microscopy of human amyloid-β deposits: characterization of parenchymal amyloid, diffuse plaques, and vascular

Rob J A Nabuurs1, Remco Natté, Fenna M de Ronde

  • 1Department of Radiology, Leiden University Medical Center, Leiden, The Netherlands. R.J.A.Nabuurs@LUMC.nl

Journal of Alzheimer'S Disease : JAD
|January 24, 2013
PubMed

Insights

Magnetic resonance imaging (MRI) can detect fibrillar amyloid-β (Aβ) deposits in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA). Non-fibrillar Aβ deposits, however, are not detectable by current MRI techniques.

Area of Science:

  • Neuroimaging
  • Neuropathology
  • Biochemistry

Background:

  • Cerebral amyloid-β (Aβ) peptide deposits are key markers of Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA).
  • Aβ aggregates into insoluble fibrils in plaques and vascular amyloid, or exists as non-fibrillar diffuse plaques.
  • Previous research suggests magnetic resonance imaging (MRI) can detect amyloid plaques, potentially due to Aβ or associated iron.

Purpose of the Study:

  • To investigate the MRI properties of different cerebral Aβ deposit types, including diffuse plaques and vascular amyloid.
  • To differentiate MRI signal changes associated with fibrillar versus non-fibrillar Aβ.
  • To inform the development of quantitative MRI methods for AD and CAA detection.

Main Methods:

  • Postmortem brain sections from AD, CAA, and Down's syndrome patients were analyzed.
  • High-resolution T2*- and T2-weighted MRI scans were acquired using a microcoil on a 9.4T MRI system.
  • MRI data were co-registered with Congo Red and Aβ-immunostainings to correlate imaging signals with Aβ morphology.

Main Results:

  • Fibrillar Aβ, found in vascular and parenchymal amyloid, significantly altered T2* and T2 values.
  • MRI signal changes in cerebral amyloid angiopathy were not consistent across all affected vessels.
  • Non-fibrillar diffuse plaques did not produce detectable changes in MRI signals.

Conclusions:

  • Only fibrillar forms of cerebral amyloid-β induce detectable MRI signal changes.
  • Non-fibrillar Aβ deposits are currently undetectable by MRI.
  • Findings are crucial for interpreting and advancing MRI techniques for Alzheimer's disease and cerebral amyloid angiopathy diagnosis and monitoring.

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