White matter hyperintensities in Alzheimer's disease: Beyond vascular contribution
Antoine Garnier-Crussard1,2,3, François Cotton4,5, Pierre Krolak-Salmon2,3
1Normandie Univ, UNICAEN, INSERM, U1237, PhIND "Physiopathology and Imaging of Neurological Disorders," Neuropresage Team, Cyceron, Caen, France.
Abstract:
White matter hyperintensities (WMH), frequently seen in older adults, are usually considered vascular lesions, and participate in the vascular contribution to cognitive impairment and dementia. However, emerging evidence highlights the heterogeneity of WMH pathophysiology, suggesting that non-vascular mechanisms could also be involved, notably in Alzheimer's disease (AD). This led to the alternative hypothesis that in AD, part of WMH may be secondary to AD-related processes. The current perspective brings together the arguments from different fields of research, including neuropathology, neuroimaging and fluid biomarkers, and genetics, in favor of this alternative hypothesis. Possible underlying mechanisms leading to AD-related WMH, such as AD-related neurodegeneration or neuroinflammation, are discussed, as well as implications for diagnostic criteria and management of AD. We finally discuss ways to test this hypothesis and remaining challenges. Acknowledging the heterogeneity of WMH and the existence of AD-related WMH may improve personalized diagnosis and care of patients.
Insights
White matter hyperintensities (WMH) in Alzheimer's disease (AD) may stem from AD-related processes, not just vascular issues. Recognizing this heterogeneity can improve personalized AD diagnosis and care.
Area of Science:
- Neurology
- Neuroscience
- Pathophysiology
Background:
- White matter hyperintensities (WMH) are common in older adults and linked to cognitive decline.
- Traditionally, WMH are viewed as vascular lesions contributing to cognitive impairment and dementia.
- Emerging evidence suggests non-vascular mechanisms, particularly in Alzheimer's disease (AD).
Purpose of the Study:
- To explore the hypothesis that some WMH in AD are secondary to AD-related processes.
- To synthesize evidence from neuropathology, neuroimaging, biomarkers, and genetics supporting this hypothesis.
- To discuss implications for AD diagnosis and management.
Main Methods:
- Review and synthesis of existing research from multiple scientific fields.
- Discussion of potential underlying mechanisms, including neurodegeneration and neuroinflammation.
- Exploration of diagnostic and therapeutic implications.
Main Results:
- Evidence supports the heterogeneity of WMH pathophysiology in AD.
- Potential AD-related mechanisms contributing to WMH are identified.
- The concept of AD-related WMH is presented as a plausible alternative or complementary explanation.
Conclusions:
- WMH in AD may arise from both vascular and AD-specific pathological processes.
- Acknowledging AD-related WMH can refine diagnostic criteria and treatment strategies for AD patients.
- Further research is needed to fully elucidate and validate the role of AD-related mechanisms in WMH.
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