Abstract Body: Introduction:
Tau deposition in pericentral sensorimotor cortex occurs later in Alzheimer's disease (AD), while cortical leptomeningeal amyloid and subsequent perivascular tau in cerebral lobes are early and characteristic features of cerebral amyloid angiopathy (CAA). We explored whether tau deposition in pericentral cortex helped distinguish CAA from AD.
Methods:
We consecutively enrolled 80 CAA cases (diagnosed with probable CAA according to modified Boston criteria version 1.5, 31 CAA-intracerebral hemorrhage, 38 CAA-cognitive decline and 11 CAA-related inflammation), 24 controls and 99 AD cases from a single medical center in China between May 2019 and August 2023. Participants completed the neuropsychological examination, brain MRI scan for evaluation of imaging markers for cerebral small vessel disease (CSVD) and neurodegeneration, and 18F-florbetapir and 18F-florzolotau PET/CT for estimation of amyloid and tau burden. We compared differences of tau-PET retention in precentral, postcentral, supplementary motor area (SMA) and paracentral gyri between CAA and controls as well as AD in region of interest analyses adjusted by age and sex, and examined the association of tau-PET retention and CAA-featured CSVD markers.
Results:
Patients with CAA showed a globally increased tau-PET retention compared to normal controls (SUVr 1.17±0.03 vs. 0.97±0.01, P<0.001), but decreased tau-PET retention compared to AD (SUVr 1.36±0.05, P=0.001). The relative values of tau-PET SUVr (gyrus/global SUVr) in precentral (0.92±0.01 vs. 0.84±0.01, P<0.001), postcentral (0.91±0.01 vs. 0.80±0.02, P<0.001), SMA (0.97±0.02 vs. 0.84±0.02, P<0.001) and paracentral (0.97±0.02 vs. 0.76±0.02, P<0.001) gyri of CAA were significantly elevated compared to those of AD. Tau-PET retentions were higher in cases with CAA-cognitive decline than cases with CAA-intracerebral hemorrhage (P < 0.01). There were significant correlations between tau SUVr in four pericentral regions and cortical superficial siderosis extent, CAA imaging score and amyloid SUVr, but not global cortical atrophy score after adjusted by sex, age and clinical subtypes in CAA (P < 0.05), which was not found in AD.
Conclusions:
These results suggest that increased pericentral tau deposition ratio might distinguish CAA from AD, and is more related to cortical CSVD pathology in CAA.