Is cerebral glucose metabolism related to blood–brain barrier dysfunction and intrathecal IgG synthesis in Alzheimer disease?

Abstract

The aim of this study was to investigate the relationships between blood–brain barrier (BBB) dysfunction, intrathecal IgG synthesis, and brain glucose consumption as detectable by means of serum/cerebrospinal fluid (CSF) albumin index (Qalb) and IgG index [(CSF IgG/serum IgG) × Serum albumin/CSF albumin)] and 2-deoxy-2-(18F) fluoro-d-glucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) in a selected population affected by Alzheimer disease (AD). The study included 134 newly diagnosed AD patients according to the NINCDS-ADRDA criteria. The mean (±SD) age of the patients was 70 (±6) years; 60 were male and 64 were female. Mini mental State Examination was equal to 18.9 (±7.2). All patients underwent a CSF assay and magnetic resonance before 18F-FDG PET scanning. The relationships were evaluated by means of statistical parametric mapping (SPM8). We found a significant negative correlation between the increase of Qalb and 18F-FDG uptake in the Brodmann Area 42 and 22 that corresponds to the left superior temporal gyrus, with higher Qalb values being related to a reduced glucose consumption in these areas. No significant relationships have been found between brain glucose consumption and IgG index. The results of our study suggest that BBB dysfunction is related to reduction of cortical activity in the left temporal cortex in AD subjects.

Alzheimer's disease and metabolic syndrome: A link from oxidative stress and inflammation to neurodegeneration

“…As well as occurring with insulin signaling, it has been found that impairment of cerebral glucose metabolism could occur in the early stages of AD, and deteriorate with the progression of the disease (Shah, Desilva, & Abbruscato, ; Chen, Deng, Zhang, & Gong, ). Compared to peripheral organs, the availability of glucose and other nutrients for neural tissues is limited by the dynamic restrictive properties of the BBB (Chiaravalloti et al, ; Keeney, Ibrahimi, & Zhao, ). Because neurons are unable to synthesize or store glucose, they are completely dependent on glucose transport across the BBB, which is facilitated by glucose transporters (GLUTs) and sodium‐dependent glucose transporters (secondary active transport; SGLT), each with different kinetic properties.…”

Metabolic Syndrome Exacerbates the Recognition Memory Impairment and Oxidative‐Inflammatory Response in Rats with an Intrahippocampal Injection of Amyloid Beta 1–42

“…Alzheimer disease (AD) is the most common cause of dementia and cognitive disorders and is one of the most important causes of morbidity and mortality among the aging population [ 17 ]. It is characterized by extracellular senile plaques of A β peptides and intracellular neurofibrillary tangles of tau protein [ 18 , 19 ]. Diverse factors have been related to AD development, but OS and inflammation invariably are involved [ 13 , 14 ].…”

The Brain Metabolic Correlates of the Main Indices of Neuropsychological Assessment in Alzheimer’s Disease

“…In particular, data concerning the relationship between glucose metabolism and common neuropsychological assessment are poor, even if the results of the neuropsychological tests may be considered as statistical parameters in research papers that include brain data analysis, by using computer-aided metrics such as statistical parametric mapping (SPM) [ 8 , 9 ].…”