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Basic Science and Pathogenesis.

S Dahyun Park1, Cheryl R McCreary1, Myrlene Gee2

  • 1University of Calgary, Calgary, AB, Canada.

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Summary
This summary is machine-generated.

Cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD) show impaired glymphatic clearance and reduced cerebrovascular reactivity (CVR). These vascular changes in CAA and AD may stem from altered blood flow dynamics rather than dilation capacity.

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Area of Science:

  • Neuroimaging
  • Neurology
  • Cerebrovascular diseases

Background:

  • Cerebral amyloid angiopathy (CAA) involves amyloid-beta deposition in brain blood vessels, increasing hemorrhage and dementia risk, and is common in Alzheimer's disease (AD).
  • Impaired glymphatic clearance and reduced cerebrovascular reactivity (CVR) are hypothesized contributors to amyloid-beta deposition.
  • Previous studies have not investigated these factors concurrently in patients with CAA or AD.

Purpose of the Study:

  • To investigate glymphatic function and CVR in patients with CAA and AD.
  • To explore the relationship between glymphatic function and CVR in these patient groups.

Main Methods:

  • MRI including diffusion tensor imaging along the perivascular space (DTI-ALPS) and BOLD imaging with hypercapnic challenge was performed on 43 CAA patients, 16 AD patients, and 53 healthy controls (HC).
  • Glymphatic function was quantified using DTI-ALPS, and CVR was measured as the percentage change in BOLD signal per mmHg increase in end-tidal CO2.
  • Statistical analyses adjusted for age, sex, and hypertension.

Main Results:

  • Patients with CAA and AD exhibited significantly lower DTI-ALPS and CVR compared to HC (p < 0.001).
  • No significant association was found between DTI-ALPS and grey matter, white matter, or global CVR in the studied groups.
  • CAA and AD participants were predominantly male, older, and had higher hypertension rates than HC.

Conclusions:

  • Reduced glymphatic function in CAA and AD is associated with cerebrovascular changes.
  • Vascular contributions to impaired glymphatic function in CAA and AD may be linked to altered vasomotion and blood flow pulsatility, not solely dilation capacity.