hide
Free keywords:
-
Abstract:
Alzheimer's disease (AD) is the most common cause for cognitive dysfunction at high age. In AD, pathological hallmarks such as beta-amyloid (Aß) aggregation and also neurometabolic change, as indicated by altered myo-inositol (mI) and N-acetylaspartate (NAA) levels, typically precede manifestation of cognitive dysfunction by years. While cerebrovascular disease occurs at earliest stages of AD pathogenesis, the interplay between vascular and neurometabolic brain change is largely unknown.
Thirty cognitively normal elderly persons (age=70±5.6 years, MMSE=29.2±1) received 11-C-Pittsburgh Compound B PET for estimating Aß-plaque density, 7 Tesla (7T) fluid-attenuated inversion recovery MRI for quantifying white matter hyperintensity volume, and high-resolution FIDLOVS-based magnetic resonance spectroscopic imaging (MRSI) at 7T to investigate tissue-specific neurometabolism in the posterior cingulate and precuneus (PCP).
Beta-amyloid (ß=0.45, p=0.018) and white matter hyperintensities (ß=0.40, p=0.046) were independently and interactively (ß= -0.49, p=0.026) associated with a higher ratio of mI over NAA (mI/NAA) in PCP gray matter but not in white matter.
Our data suggest that cerebrovascular disease and Aß burden are synergistically related to AD-related gray matter neurometabolism at high age.
