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Cortical microinfarcts and demyelination significantly affect cognition in brain aging
Enikö Kövari1, Gabriel Gold, François R Herrmann
1Department of Psychiatry, HUG Belle-Idée, University of Geneva School of Medicine, Geneva, Switzerland. eniko.kovari@hcuge.ch
Stroke
|January 7, 2004
Summary
Microvascular lesions like cortical microinfarcts and white matter demyelination significantly worsen cognitive function in aging brains. Focal glioses, however, show no clinical impact on cognition.
Area of Science:
- Neurology
- Neuroscience
- Pathology
Background:
- Microvascular lesions are prevalent in aging brains, but their clinical significance is debated.
- Previous studies faced methodological challenges, including confounding pathologies.
- This study focused on elderly individuals with cognitive impairment but excluded major neurodegenerative or vascular pathologies.
Purpose of the Study:
- To prospectively evaluate the cognitive consequences of specific microvascular lesions in aging.
- To determine the predictive value of different neuropathological findings for cognitive status.
Main Methods:
- Clinicopathological study of 45 elderly individuals.
- Prospective cognitive assessment using the Clinical Dementia Rating (CDR) scale.
- Neuropathological analysis including Abeta deposition, cortical microinfarcts, glioses, and demyelination.
Main Results:
- Cortical microinfarcts were the strongest predictor of cognitive status (19.9% CDR variability) after controlling for age and Abeta.
- Periventricular and diffuse white matter demyelination also significantly predicted cognitive status.
- Combined, these microvascular lesions explained 27.9% of clinical variability; focal glioses did not correlate with cognitive outcome.
Conclusions:
- Cortical microinfarcts and white matter demyelination are key contributors to cognitive decline in brain aging.
- Neuropathological assessment of focal cortical and white matter gliosis lacks clinical validity for cognitive status.