Level of education modulates the impact of tau-pathology on neuronal function

Ziel/Aim:

Since PET imaging studies have consistently demonstrated a close relationship between tau-pathology and changes in glucose metabolism (i.e. neuronal dysfunction), we investigated whether this relationship is influenced by the level of education in a group of patients with Alzheimer's disease (AD).

Methodik/Methods:

We included 38 patients with mild-to-moderate AD (M(Age)= 67.05 years, M(MMSE)= 23.89 points, M(Education)= 13.72 years), for whom a [¹⁸F]AV-1451 (i.e. tau-pathology measure) and [¹⁸F]FDG scan (i.e. measure for neuronal function) were available. The pre-processed PET scans were z-transformed using a [¹⁸F]AV-1451 and [¹⁸F]FDG template of a healthy control sample, and subsequently thresholded at a z-score of z >= 3.0, representing a one-tailed p-value of p = 0.001. Next, three volumes were computed for each patient: the tau-specific (i.e. tau-pathology in absence of neuronal dysfunction), the FDG-specific (i.e. neuronal dysfunction without tau-pathology), and the overlap volume (i.e. tau-pathology and neuronal dysfunction). Mean z-scores and volume sizes were extracted, respectively, and used as dependent variables in regression analyses with education as predictor, and age and MMSE as covariates.

Ergebnisse/Results:

Years of education were positively associated with the tau-specific volume size (b = 0.390, t(34)= 2.454, p = 0.019) meaning that higher educated patients presented a more extended tau-pathology pattern in absence of regional neuronal dysfunction. Concomitantly, education was positively related with tau-pathology load in the overlap region (b = 0.328, t(34)= 2.187, p = 0.036) suggesting that more tau-pathology is necessary to provoke neuronal dysfunction at higher levels of education.

Schlussfolgerungen/Conclusions:

At higher education, tau-pathology is less paralleled by regional neuronal dysfunction. Presumably, early lifetime factors such as education support resilience mechanisms, which potentially ameliorate disease-related effects late in life.