The Biological Substrate of the Motoric Cognitive Risk Syndrome: A Pilot Study Using Amyloid-/Tau-PET and MR Imaging

Abstract

A cross-sectional pilot study to explore the biological substrate of the Motoric Cognitive Risk (MCR) syndrome in a Memory Clinic cohort, using a multimodal imaging approach, was conducted. Twenty participants were recruited and classified as MCR+/−. Amyloid- and tau-PET uptakes, temporal atrophy, white matter hyperintensities, lateral ventricular volume (LVV), and diffusion tensor parameters were compared between groups. No significant differences were found in imaging features related to Alzheimer’s disease or gross vascular damage. MCR+ patients had increased LVV and altered diffusion parameters in the superior corona radiata. Ventricular enlargement and microstructural damage of the surrounding white matter tracts could contribute to MCR pathophysiology.

Associations between blood-based biomarkers of Alzheimer’s disease with cognition in motoric cognitive risk syndrome: A pilot study using plasma Aβ42 and total tau

“…Therefore, clarifying the relationship between AD pathology and MCR may aid clinical diagnosis and the planning of prevention strategies. To date, only one study has investigated the relationship between MCR and AD pathology using imaging biomarkers (Bommarito et al, 2022) and reported findings inconsistent with the present study. In the above mentioned study, 20 patients with cognitive complaints (8 individuals with MCR and 12 without MCR) were recruited from the Memory Center of the Geneva University Hospitals, and no significant differences in the deposition of amyloid and tau protein in the brain between older adults with MCR and without MCR were found.…”

“…For cognitively normal individuals, earlier studies have reported significant correlations between slow gait speed and amyloid deposition in the subcortical and cortical areas (Del Campo et al, 2016;Wennberg et al, 2017). However, recent studies did not find increased amyloid deposition in older adults with MCR (Bommarito et al, 2022;Gomez et al, 2022). In this study, for the first time, we compared plasma Aβ42 among older adults with NC, individuals with MCR and those with AD.…”

“…In the above mentioned study, 20 patients with cognitive complaints (8 individuals with MCR and 12 without MCR) were recruited from the Memory Center of the Geneva University Hospitals, and no significant differences in the deposition of amyloid and tau protein in the brain between older adults with MCR and without MCR were found. The individuals without MCR in Bommarito et al (2022) had subjective cognitive complaints and a CDR scale score of 0.5, which might have affected the results of the study. The strength of our study was that NC and AD groups were included for comparison.…”

“…We also noted that there were no significant correlations between the level of plasma Aβ42 and cognitive function in the MCR group. Previous studies suggested that the pathophysiological mechanisms underlying MCR were probably heterogeneous ( Bommarito et al, 2022 ). Gomez et al (2022) recruited 204 participants with MCR and noted that MCR was associated with prominent white matter abnormalities and frontoparietal atrophy.…”

“…Alzheimer’s disease pathology has been found to have a strong association with gait disorder in older adults without dementia and can predict cognitive decline and incident dementia ( Del Campo et al, 2016 ; Tian et al, 2017 ). Recently, in a study investigating the relationships between MCR and AD pathology using imaging biomarkers, no significant differences in the biomarkers of AD, such as amyloid, tau deposition, or white matter hyperintensities, were found between individuals with MCR and without MCR ( Bommarito et al, 2022 ). Although the findings of this study were informative, the sample size was relatively small, and no comparisons were made with the normal cognition (NC) group, making it difficult to determine whether the physiological changes in MCR were caused by normal aging or the pathological changes related to AD.…”