Publication
Previous research has revealed patterns of brain atrophy in subjective cognitive decline, a potential preclinical stage of Alzheimer's disease. However, the involvement of myelin content and microstructural alterations in subjective cognitive decline has not previously been investigated. This study included three groups of participants recruited from the Compostela Aging Study project: 53 cognitively unimpaired adults, 16 individuals with subjective cognitive decline and hippocampal atrophy and 70 with subjective cognitive decline and no hippocampal atrophy. Group differences were analysed across five MRI biomarkers derived from multi-component T2 relaxometry, each sensitive to variations in cerebral composition and microstructural tissue integrity. Although no significant differences in myelin content were observed between groups, the subjective cognitive decline with hippocampal atrophy group exhibited a larger free-water fraction, and reduced fraction and relaxation times of the intra/extracellular water compartment in frontal, parietal and medial temporal lobe brain regions and white matter tracts as compared with the other groups. Moreover, both subjective cognitive decline groups displayed lower total water content as compared with the control group and the subjective cognitive decline with hippocampal atrophy group showed lower total water content as compared with the subjective cognitive decline without hippocampal atrophy group. These changes are likely related to microstructural tissue differences related to neuroinflammation, axonal degeneration, iron accumulation or other physiologic variations, calling for further examinations. Cerebral composition and microstructural tissue integrity in individuals with subjective cognitive decline were examined. Although no group differences in myelin content were found, participants with evidence of hippocampus atrophy exhibited altered water compartment biomarkers, suggesting neuroinflammation, axonal degeneration, or iron deposition, highlighting microstructural changes potentially linked to Alzheimer's disease progression.