A comparative study of posterior cingulate metabolism in patients with mild cognitive impairment due to Parkinson's disease or Alzheimer's disease.

Few comparative studies have assessed metabolic brain changes in cognitive impairment among neurodegenerative disorders, and the posterior cingulate cortex (PCC) is a metabolically active brain region with high involvement in multiple cognitive processes. Therefore, in this study, metabolic abnormalities of the PCC were compared in patients with mild cognitive impairment (MCI) due to Parkinson's disease (PD) or Alzheimer's disease (AD), as examined by proton magnetic resonance spectroscopy (H-MRS). Thirty-eight patients with idiopathic PD, including 20 with mild cognitive impairment (PDMCI) and 18 with normal cognitive function (PDN), 18 patients with probable mild cognitive impairment (ADMCI), and 25 healthy elderly controls (HCs) were recruited and underwent PCC H-MRS scans. Compared with HCs, patients with PDMCI exhibited significantly reduced concentrations of N-acetyl aspartate (NAA), total NAA (tNAA), choline (Cho), glutathione (GSH), glutamate + glutamine (Glx) and total creatine (tCr), while ADMCI cases exhibited significantly elevated levels of myo-inositol (Ins) and Ins/tCr ratio, as well as reduced NAA/Ins ratio. No significant metabolic changes were detected in PDN subjects. Compared with ADMCI, reduced NAA, Ins and tCr concentrations were detected in PDMCI. Besides, ROC curve analysis revealed that tCr concentration could differentiate PDMCI from PDN with an AUC of 0.71, and NAA/Ins ratio could differentiate patients with MCI from controls with normal cognitive function with an AUC of 0.74. Patients with PDMCI and ADMCI exhibited distinct PCC metabolic H-MRS profiles. The findings suggested cognitively normal PD patients with low NAA and tCr in the PCC might be at risk of preclinical PDMCI, and Ins and/or NAA/MI ratio in the PCC should be reconsidered a possible biomarker of preclinical MCI in clinical practice. So, comparing PCC's H-MRS profiles of cognitive impairment among neurodegenerative illnesses may provide useful information for better defining the disease process and elucidate possible treatment mechanisms.