2024-Abstract-1

by | Sep 10, 2024 | 2024 Abstracts

Abstract 1
Category: Basic Science

At the end of the session, participants will be able to:

  1. To become aware of the difference between progression of amyloid plaques and cerebral amyloid angiopathy when comparing cerebral and cerebellar cortices.
  2. To become aware of the decoupling of meningeal and parenchymal vascular amyloid deposits in the cerebellum, but not in the cerebral cortex.

COI Disclosure:

None to disclose.

Presenter

David Munoz is a neuropathologist at St. Michael’s hospital, Unity Health Toronto.

David G. Munoz1,3, Julia Keith2,3, Sara Mitchell4, Mario Masellis4, Alyona Ivanova5, Sandra Black4

  1. Department of Laboratory Medicine, St. Michael’s Hospital, Unity Health Toronto
  2. Department of Anatomic Pathology, Sunnybrook Health Sciences Center
  3. Department of Laboratory Medicine & Pathobiology, University of Toronto
  4. Division of Neurology, Sunnybrook Health Sciences Center
  5. 5.Institute of Medical Science, University of Toronto

Target Audience:
Pathologists, Residents

CanMEDS:
Medical Expert (the integrating role), Communicator, Scholar, Professional

Distinctive pattern of cerebral amyloid angiopathy in the cerebellum

Abstract

We aimed to compare the patterns of cerebral amyloid angiopathy (CAA) in the cerebral and cerebellar cortices. We studied 24 brains from the pathology departmental archives at Sunnybrook, ages 56-93. Diagnoses included Alzheimer’s disease and vascular dementia. Meningeal, parenchymal, and capillary CAA were evaluated in frontal, occipital, and basal temporal cortices, and cerebellum. CAA and plaques were scored 0-3 as per Love 2014. CAA was identified in 21/24 cases. Cerebellum CAA was present in 17/24 cases; it was never present without some CAA in one of the neocortical regions. However, the cerebellar CAA score exceeded the score in any neocortical region in 4 cases, was equal in 9, and less than at least one neocortical region in 7. In the cerebellum meningeal exceeded parenchymal scores in 12 cases, and parenchymal exceeded meningeal in 5 cases. Cerebellar CAA with scores of up to 3 was present in cases without cerebellar plaques; likewise cerebellar plaque scores of 2 were present in a case without cerebellar CAA. There never was capillary CAA in the absence of parenchymal CAA in any region. There was no correlation between meningeal and parenchymal CAA scores in the cerebellum, whereas they were highly correlated in neocortical areas. We conclude that cerebellar CAA is common, often equal or more severe than neocortical CAA. In the cerebellum, unlike in the neocortex, meningeal and parenchymal CAA are not correlated, suggesting that they are responses to largely independent pathophysiological mechanisms.