The objective of this paper is to examine the relationship between the development of executive function (EF) and obesity in children and adolescents. We reviewed 1,065 unique abstracts: 31 from PubMed, 87 from Google Scholar, 16 from Science Direct, and 931 from PsycINFO. Of those abstracts, 28 met inclusion criteria and were reviewed. From the articles reviewed, an additional 3 articles were added from article references (N = 31). Twenty-three studies pertained to EF (2 also studied the prefrontal and orbitofrontal cortices (OFCs); 6 also studied cognitive function), five studied the relationship between obesity and prefrontal and orbitofrontal cortices, and three evaluated cognitive function and obesity. Inhibitory control was most often studied in both childhood (76.9%) and adolescent (72.7%) studies, and obese children performed significantly worse (P < 0.05) than healthy weight controls on various tasks measuring this EF domain. Although 27.3% of adolescent studies measured mental flexibility, no childhood studies examined this EF domain. Adolescents with higher BMI had a strong association with neurostructural deficits evident in the OFC. Future research should be longitudinal and use a uniform method of EF measurement to better establish causality between EF and obesity and consequently direct future intervention strategies.

Inflammation has been implicated in the pathology of several neurodegenerative diseases, including Parkinson’s disease (PD). Studies using the endotoxin lipopolysaccharide (LPS), a potent inflammogen, show that systemic insults can trigger prolonged microglial activation and pro-inflammatory cytokine production leading to degeneration of substantia nigra (SN) dopamine (DA) neurons, mimicking idiopathic PD. Because rapid effects of LPS on SN neurons had not been investigated previously, the focus of this study is to assess time-dependent alterations in SN neuroinflammation, DAergic neurons, and neuronal signaling cascades following LPS administration. LPS (5 mg/kg, i.p.) or saline (0.9% NaCl) was administered to 8-month-old male mice. At 3hrs, 5hrs, and 12hrs post-injection, the morphology of the SN was assessed using antibodies directed against tyrosine hydroxylase (TH, DAergic marker), Iba-1 (pan-microglial marker), phospho-ERK, and phospho-CREB (signaling). LPS administration significantly reduced TH-immunoreactivity (ir) at all time-points with the greatest reduction observed at 12 h post-injection. Reduced TH-ir was accompanied by a significant increase in activated microglia at all time-points following LPS. By 12 h post-injection, LPS-treated mice exhibited activated as well as reactive microglia, which can result in neuronal damage. These data demonstrate that the initial reduction in TH-ir observed after an LPS injection was not concomitant with morphological alterations in microglial cells, even though a significant increase in phospho-ERK was observed in glial cells as soon as 3 h post-injection. It is possible that the initial alteration in DA phenotype (TH reduction) may perpetuate an inflammatory response that persists and leads to further DAergic damage.