Banks of the Superior Temporal Sulcus in Alzheimer’s Disease: A Pilot Quantitative Susceptibility Mapping Study

Abstract

Background: Brain iron homeostasis is disrupted in neurodegeneration and areas of iron overload partially overlap with regions of amyloid and tau burden in Alzheimer’s disease (AD). Previous studies demonstrated alterations in brain iron accumulation in AD using quantitative susceptibility mapping (QSM). Objective: Here, we investigate brain alterations of QSM values in AD and non-AD patients as compared to healthy controls (HC) in the superior temporal sulcus and its banks (BANKSSTS), one of the top AD-affected regions. Methods: Thirty-four patients who underwent brain MRI including a multi-echo gradient-echo sequence were subdivided into AD (n = 19) and non-AD (n = 15) groups according to their clinical profile, CSF (Aβ 42/40) and/or amyloid-PET status. Ten HC were also included. QSM values were extracted from left and right BANKSSTS and compared among groups. Correlation and binomial regression analyses between QSM values and CSF-AD biomarkers were conducted. Results: QSM in left BANKSSTS was significantly different among groups (p = 0.003, H = 11.40), being higher in AD. QSM values in left BANKSSTS were correlated with Aβ 42 (rho –0.55, p = 0.005), Aβ 42/40 (rho –0.66, p < 0.001), pTau (rho 0.63, p < 0.001), tTau (rho 0.56, p = 0.005), tTau/Aβ 42 (rho 0.68, p < 0.001) and pTau/Aβ 42 (rho 0.71, p < 0.001). No correlations between QSM values and amyloid-PET SUVR in the left BANKSSTS were found. QSM values in left BANKSSTS showed good accuracy in discriminating AD (AUC = 0.80, CI95 % [0.66–0.93]). Higher QSM values were independent predictors of Aβ 42 (B = 0.63, p = 0.032), Aβ 42/40 (B = 0.81, p = 0.028), pTau (B = 0.96, p = 0.046), tTau (B = 0.55, p = 0.027), and tTau/Aβ 42 (B = 1.13, p = 0.042) positivity. Conclusion: Our preliminary data support the potential role of increased QSM values in the left BANKSSTS as an auxiliary imaging biomarker in AD diagnosis.

The Irony of Iron: The Element with Diverse Influence on Neurodegenerative Diseases

“…Both studies identify strong association between iron and tau levels possibly underlying their findings. A significant increase in iron is seen to be associated more with later stages of disease progression [22,24,73], perhaps-according to our discussion-either due to prolonged effects of iron and Aβ co-existence or due to the emergence of tau. Whether tau or iron accumulation occurs first in disease pathogenesis, the two disease pathologies seem to be more closely associated with one another along disease progression [22].…”