CSF Aβ(42) and tau in Parkinson's disease with cognitive impairment

Abstract

We tested the hypothesis that the CSF biomarker signature associated with Alzheimer's disease (AD) is present in a subset of individuals with Parkinson's disease and Dementia (PD-D) or with PD and Cognitive Impairment, Not Dementia (PD-CIND). We quantified CSF Aβ(42), total tau (T-tau), and phospho-tau (P181-tau) using commercially available kits. Samples were from 345 individuals in seven groups (n): Controls ≤50 years (35), Controls >50 years (115), amnestic Mild Cognitive Impairment (aMCI) (24), AD (49), PD (49), PD-CIND (62), and PD-D (11). We observed expected changes in AD or aMCI compared with age-matched or younger controls. CSF Aβ(42) was reduced in PD-CIND (P < 0.05) and PD-D (P < 0.01), whereas average CSF T-tau and P181-tau were unchanged or decreased. One-third of PD-CIND and one-half of PD-D patients had the biomarker signature of AD. Abnormal metabolism of Aβ(42) may be a common feature of PD-CIND and PD-D.

Figure 1. Scatter plots of CSF Aβ₄₂ and P181-tau concentrations

Individuals’ CSF Aβ₄₂ and P181-tau concentrations for (A) both Control groups, subjects with amnestic Mild Cognitive Impairment (MCI), and patients with Alzheimer’s Disease (AD), and for (B) patients with Parkinson’s disease (PD) without cognitive impairment (CI), with CI but Not Dementia (PD-CIND), or dementia (PD-D).