Introduction: Obesity and insulin resistance negatively influence neural activity and cognitive function, but electrophysiological mechanisms underlying these interrelationships remain unclear. This study investigated whether adiposity and insulin resistance moderated neural activity and underlying cognitive functions in young adults.
Methods: Real-time electroencephalography (EEG) was recorded in 38 lean (n = 12) and obese (n = 26) young adults with (n = 15) and without (n = 23) insulin resistance (18-38 years, 55.
Copper/zinc superoxide dismutase 1 (SOD1) scavenges free radicals that may otherwise damage brain parenchyma. Impaired SOD1 activity drives Alzheimer's disease (AD) neuropathology in animal models and postmortem AD brains. Yet, it is unknown how cerebrospinal fluid (CSF) SOD1 is related to AD-relevant cognitive, neuroimaging, and CSF neurotoxic factors, and what potential mechanisms underlie these associations.
View Article and Find Full Text PDFCholecystokinin (CCK) is a satiety hormone that is highly expressed in brain regions like the hippocampus. CCK is integral for maintaining or enhancing memory and thus may be a useful marker of cognitive and neural integrity in participants with normal cognition, mild cognitive impairment, and Alzheimer's disease (AD). Cerebrospinal fluid (CSF) CCK levels were examined in 287 subjects from the Alzheimer's Disease Neuroimaging Initiative.
View Article and Find Full Text PDFBackground/objective: Insulin-like growth factor binding protein 2 (IGFBP-2) regulates blood glucose levels, facilitates hippocampal synaptic plasticity and may have a predictive value for Alzheimer's disease (AD) diagnosis.
Methods: IGFBP-2 levels were studied in plasma in 566 subjects and in cerebrospinal fluid (CSF) in 245 subjects across the AD spectrum from the Alzheimer's Disease Neuroimaging Initiative (ADNI). Variants in the IGFBP-2 gene were examined.
J Alzheimers Dis
February 2018
Background: Obesity and insulin resistance are associated with neuropathology and cognitive decline in Alzheimer's disease (AD).
Objective: Ecto-nucleotide pyrophosphatase/phosphodiesterase 2, also called autotaxin, is produced by beige adipose tissue, regulates metabolism, and is higher in AD prefrontal cortex (PFC). Autotaxin may be a novel biomarker of dysmetabolism and AD.