A new study has suggested that people with type-2 diabetes, who are overweight or obese are more likely to have exacerbated and progressive abnormalities in the structure of their brains and cognition, find researchers. The new research was the result of a collaboration between Dr Sunjung Yoon and Dr In Kyoon Lyoo, both of the Ewha Brain Institute at the Ewha Womans University in Seoul, South Korea, and Hanbyul Cho, of The Brain Institute at the University of Utah in Salt Lake City. Their findings were published in Diabetologia. Evidence suggests that type-2 diabetes and obesity independently have adverse effects on many organs, including the brain. For example, type-2 diabetes is known to be associated with the progression of cognitive dysfunction and may amplify the risk of developing dementia. Scientists suggested that metabolic dysfunctions such as insulin resistance, inflammation, and poor sugar level control might all play a role in the brain alterations linked with type-2 diabetes, although exactly how this happens is not yet fully understood. Obesity can potentially pave the way for the development of further conditions, and it is connected with a greater risk of developing type-2 diabetes. Moreover, obesity has a relationship with metabolic dysfunction and may worsen the metabolic abnormalities that are associated with type 2 diabetes. Furthermore, the metabolic dysfunction that is linked to obesity may be responsible for brain alterations and cognitive impairment, regardless of the presence of type 2 diabetes. Yoon, Lyoo, Cho, and colleagues set out to explore the combined effects of obesity and type 2 diabetes on brain structure and cognitive function; they say that the rising prevalence of obesity may contribute to the global epidemic of type 2 diabetes. Participants’ brains were analyzed using MRI to evaluate the thickness of the cerebral cortex. Cognitive assessments to test memory, executive function, and psychomotor speed were also conducted, given the fact that these abilities are often affected by type-2 diabetes. The researchers revealed that when compared with people of a healthy weight, individuals with type-2 diabetes exhibited significant thinning of gray matter in the temporal, prefrontoparietal, motor, and occipital cortices of the brain. Gray matter of the temporal and motor cortices was thinner still in the obese diabetic group than in the group comprising healthy-weight diabetics. The temporal lobe, in particular, was found to be vulnerable in people with a combination of obesity and type-2 diabetes. Wasting of the temporal lobe has previously been shown to be an early indicator of Alzheimer’s disease. The region-specific changes that the researchers observed in the study may partly explain the mechanism linking obesity, type 2 diabetes, and the development of dementia. “These findings suggest that weight status may play additive roles in type 2 diabetes-related brain and cognitive alterations,” noted the researchers. “Our findings also highlight the need for early intervention aimed to reduce risk factors for overweight or obesity in type-2 diabetic individuals to preserve their brain structure and cognitive function.” While the specific factors that contribute to the brain alterations are not clear, managing insulin resistance during the early stages of type-2 diabetes could potentially make a difference. The researchers point out that the study did not include people who were overweight or obese without diabetes. “Therefore, we could not determine the potential effects of overweight/obesity that are completely independent of type-2 diabetes on metabolic, brain, and cognitive measures,” the authors concluded. Separately, a new study has found that two compounds added to tonic water may be an effective treatment for the disease. Dr Pawan Sharma, of the Woolcock Institute of Medical Research and School of Life Sciences at the University of Technology in Australia, and colleagues recently published their findings in the journal Scientific Reports. Inhaling such substances can lead to inflammation of the airways, causing symptoms such as shortness of breath, wheezing, coughing, and chest pain. To reach their findings, the researchers gave mouse models of allergic asthma intranasal doses of either chloroquine or quinine. Nearly 24 hours after administration, the lung function, airway inflammation, and airway structure of the mice were assessed upon exposure to two allergens. Not only did chloroquine and quinine prevent airway inflammation in the mice, but the bitter compounds also prevented other key characteristics of allergic asthma, including mucus accumulation and structural changes to the airway.