No abstract

Obesity is a global health problem with a broad set of comorbidities, such as malnutrition, metabolic syndrome, diabetes, systemic hypertension, heart failure, and kidney failure. This review describes recent findings of neuroimaging and two studies of cell density regarding the roles of overnutrition-induced hypothalamic inflammation in neurodegeneration. These studies provided consistent evidence of smaller cortical thickness or reduction in the gray matter volume in people with overweight and obesity; however, the investigated brain regions varied across the studies. In general, bilateral frontal and temporal areas, basal nuclei, and cerebellum are more commonly involved. Mechanisms of volume reduction are unknown, and neuroinflammation caused by obesity is likely to induce neuronal loss. Adipocytes, macrophages of the adipose tissue, and gut dysbiosis in overweight and obese individuals result in the secretion of the cytokines and chemokines that cross the blood-brain barrier and may stimulate microglia, which in turn also release proinflammatory cytokines. This leads to chronic low-grade neuroinflammation and may be an important factor for apoptotic signaling and neuronal death. Additionally, significant microangiopathy observed in rat models may be another important mechanism of induction of apoptosis. Neuroinflammation in neurodegenerative diseases (such as Alzheimer’s and Parkinson’s diseases) may be similar to that in metabolic diseases induced by malnutrition. Poor cognitive performance, mainly in executive functions, in individuals with obesity is also discussed. This review highlights the neuroinflammatory and neurodegenerative mechanisms linked to obesity and emphasizes the importance of developing effective prevention and treatment intervention strategies for overweight and obese individuals.

No abstract

Objective: This study aimed to compare cortex thickness and neuronal cell density in postmortem brain tissue from people with overweight or obesity and normal weight. Methods: The cortex thickness and neuron density of eight donors with overweight or obesity (mean 5 31.6 kg/m 2 ; SD 5 4.35; n 5 8; 6 male) and eight donors with normal weight (mean 5 21.8 kg/m 2 ; SD 5 1.5; n 5 8; 5 male) were compared. All participants were Mexican and lived in Mexico City. Randomly selected thickness measures of different cortex areas from the frontal and temporal lobes were analyzed based on high-resolution real-size photographs. A histological analysis of systematic-random fields was used to quantify the number of neurons in postmortem left and right of the first, second, and third gyri of frontal and temporal lobe brain samples. Results: No statistical difference was found in cortical thickness between donors with overweight or obesity and individuals with normal weight. A smaller number of neurons was found among the donors with overweight or obesity than the donors with normal weight at different frontal and temporal areas. Conclusions: A lower density of neurons is associated with overweight or obesity. The morphological basis for structural brain changes in obesity requires further investigation.

Cognitive impairment is a key feature of schizophrenia. While a 2019 study 1 suggested that individuals with psychosis experience a progressive decline in certain cognitive domains during the first 10 years of their illness, other clinical studies 2,3 and functional magnetic resonance imaging-based studies 4,5 have proposed that most cognitive deficits are present during the first episode and remain stable over time. To examine the temporal nature of cognitive deficits on the schizophrenia spectrum, we examined cognition in never-medicated individuals at different stages of the illness.

Background. Adults with type two diabetes mellitus (DM2) show cognitive deficits within the executive function domain. The detrimental effects of DM2 over executive function (EF) performance may be mediated by factors such as cognitive reserve (CR). CR mediates cognitive performance by delaying the appearance of clinical symptoms from subjacent brain pathology or attenuating the severity of such symptoms. Our main goal was to study the effects of CR on executive functions of adults with DM2. Methods. Data from a total of 1,034 adults were included (362 women, 672 men). Subjects were categorized into four groups: subjects with DM2 and high CR ( n = 235 ), control subjects with high CR ( n = 265 ), subjects with DM2 and low CR ( n = 298 ), and control subjects with low CR ( n = 236 ). CR was quantified through 3 proxies: education, occupational complexity, and leisure activities. Executive functions were evaluated through visual scanning, verbal fluency, and backwards counting tasks. First, a series of four one-way ANOVAs was performed where group was included as a between-subject factor and executive function as a dependent variable. Second, a hierarchical multiple regression analysis was conducted to assess the weight of each CR proxy on EF performance. Results. CR level significantly affected all executive function scores independently of the diabetes status. Hierarchical regression analyses indicated that years of education accounted for most of the variance in the model for executive function performance. In this study, we found that there is a significant effect of CR on executive function performance of DM2 subjects and education is the most important CR proxy.

We explored the neurophysiological activity underlying auditory novelty detection in antipsychotic-naive patients with a first episode of psychosis (FEP). Fifteen patients with a non-affective FEP and 13 healthy controls underwent an active involuntary attention task along with an EEG acquisition. Time-frequency representations of power, phase locking, and fronto-parietal connectivity were calculated. The P3a event-related potential was extracted as well. Compared to controls, the FEP group showed reduced theta phase-locking and fronto-parietal connectivity evoked by deviant stimuli. Also, the P3a amplitude was significantly reduced. Moreover, reduced theta connectivity was associated with more severe negative symptoms within the FEP group. Reduced activity (phase-locking and connectivity) of novelty-related theta oscillations, along with P3a reduction, may represent a failure to synchronize large-scale neural populations closely related to fronto-parietal attentional networks, and might be explored as a potential biomarker of disease severity in patients with emerging psychosis, given its association with negative symptoms.

No abstract