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Alzheimer's Imaging Consortium.

Laura E Jonkman1, Niels Reijner1, Maud M A Bouwman1

  • 1Amsterdam UMC, location VUmc, Amsterdam, Netherlands.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
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Summary
This summary is machine-generated.

Postmortem MRI accurately reflects in-vivo imaging in neurodegenerative diseases. This study links brain atrophy and protein pathology to cognitive decline, improving diagnostic and therapeutic strategies for conditions like Alzheimer's disease.

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Area of Science:

  • Neuroscience
  • Radiology
  • Pathology

Background:

  • Dementia encompasses neurodegenerative diseases like Alzheimer's disease (AD), Lewy body dementia (LBD), and Frontotemporal dementia (FTD).
  • These diseases are characterized by the accumulation of misfolded proteins, leading to neuronal dysfunction and cognitive decline.
  • There is a critical need for non-invasive, pathology-sensitive neuroimaging biomarkers to define disease states and monitor progression.

Purpose of the Study:

  • To correlate in-situ postmortem MRI findings with detailed neuropathology in individuals with neurodegenerative diseases.
  • To validate postmortem MRI as a proxy for in-vivo imaging in dementia.
  • To identify imaging biomarkers associated with specific protein pathologies and neurodegenerative processes.

Main Methods:

  • Utilized a unique within-subject correlative postmortem in-situ MRI and neuropathology approach in over 100 brain donors.
  • Applied MRI techniques including cortical thickness, microstructural integrity, and connectome analysis.
  • Performed digital quantitative pathology for amyloid-beta (Aβ), phosphorylated tau (pTau), alpha-synuclein (α-synuclein), and TDP-43 inclusions, alongside markers for neuroinflammation, myelin, neuro-axonal degeneration, and synaptic density.

Main Results:

  • Postmortem in-situ MRI serves as a reliable proxy for antemortem in-vivo MRI.
  • Cortical atrophy patterns in AD correlate with Aβ plaques and neuro-axonal damage.
  • T1w/T2w ratio indicates broader cortical integrity beyond myelin.
  • Late co-pathology in AD and LBD exacerbates amygdala and hippocampal volume loss.
  • Increased α-synuclein pathology in LBD is linked to widespread brain network reorganization.
  • Hippocampal subfield vulnerability to protein aggregation and synaptic degeneration correlates with MRI volume loss and cognitive outcomes.
  • Cell loss in mono-aminergic and cholinergic nuclei is associated with microstructural alterations and cortical projections.

Conclusions:

  • Integrating clinical, radiological, and histopathological data enhances understanding of neurodegenerative diseases.
  • This approach yields fundamental knowledge for improved interpretation of imaging datasets.
  • Findings pave the way for more accurate disease definition, progression monitoring, and treatment strategies.