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Research Paper|Volume 13, Issue 16|pp 19963—19977

The interplay between gray matter and white matter neurodegeneration in subjective cognitive decline

Nira Cedres1,2, Patricia Diaz-Galvan1,3, Lucio Diaz-Flores4, J-Sebastian Muehlboeck1, Yaiza Molina5, José Barroso6, Eric Westman1,7, Daniel Ferreira1,3,6
  • 1Division of Clinical Geriatrics, Centre for Alzheimer Research, Department of Neurobiology, Care Sciences, and Society (NVS), Karolinska Institutet (KI), Stockholm, Sweden
  • 2Department of Psychology, Sensory Cognitive Interaction Laboratory (SCI-lab), Stockholm University, Stockholm, Sweden
  • 3Department of Radiology, Mayo Clinic, Rochester, MN 55905, USA
  • 4Hospital Universitario de Canarias, La Laguna, Tenerife, Spain
  • 5Faculty of Health Sciences, University Fernando Pessoa Canarias, Las Palmas de Gran Canaria, Spain
  • 6Faculty of Psychology, University of La Laguna, La Laguna, Tenerife, Spain
  • 7Department of Neuroimaging, Centre for Neuroimaging Sciences, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, London, UK
* Shared senior authorship
Received: January 12, 2021Accepted: August 14, 2021Published: August 25, 2021
https://doi.org/10.18632/aging.203467

Copyright: © 2021 Cedres et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Aims: To investigate the interplay between gray matter (GM) and white matter (WM) neurodegeneration in subjective cognitive decline (SCD), including thickness across the whole cortical mantle, hippocampal volume, and integrity across the whole WM.

Methods: We included 225 cognitively unimpaired individuals from a community-based cohort. Subjective cognitive complaints were assessed through 9 questions covering amnestic and non-amnestic cognitive domains. In our cohort, 123 individuals endorsed from one to six subjective cognitive complaints (i.e. they fulfilled the diagnostic criteria for SCD), while 102 individuals reported zero complaints. GM neurodegeneration was assessed through measures of cortical thickness across the whole mantle and hippocampal volume. WM neurodegeneration was assessed through measures of mean diffusivity (MD) across the whole WM skeleton. Mediation analysis and multiple linear regression were conducted to investigate the interplay between the measures of GM and WM neurodegeneration.

Results: A higher number of complaints was associated with reduced hippocampal volume, cortical thinning in several frontal and temporal areas and the insula, and higher MD across the WM skeleton, with a tendency to spare the occipital lobe. SCD-related cortical thinning and increased MD were associated with each other and jointly contributed to complaints, but the contribution of cortical thinning to the number of complaints was stronger.

Conclusions: Neurodegeneration processes affecting the GM and WM seem to be associated with each other in SCD and include brain areas other than those typically targeted by Alzheimer’s disease. Our findings suggest that SCD may be a sensitive behavioral marker of heterogeneous brain pathologies in individuals recruited from the community.