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Alzheimer's and obesity

Obesity and ageing linked to Alzheimers disease

The researchers discovered that certain areas of the brain respond differently to risk factors associated with Alzheimer's disease

When a high-fat, high-sugar diet that leads to obesity is paired with normal aging, it may contribute to the development of Alzheimer's disease, according to researchers from Brock University in Ontario, Canada. In addition, the researchers discovered that certain areas of the brain respond differently to risk factors associated with Alzheimer's.

Alzheimer's disease, the most common form of dementia, is a progressive brain disorder that leads to loss of cognitive skills and memory and causes significant changes in behavior. Aging is a significant risk factor for Alzheimer's. Previous studies suggest that diet-related obesity is also associated with development of the disease.

The study, ‘Evaluation of neuropathological effects of a high-fat high-sucrose diet in middle-aged male C57BL6/J mice’, published in Physiological Reports, notes that looked at the effects of an obesity-inducing diet on insulin signalling (the process that tells the body how to use sugar), and markers of inflammation and cellular stress. These factors have been found to be involved in the progression of Alzheimer's disease during the aging process in mice.

One group of mice received a high-fat, high-sugar diet (HFS), while the control group ate a normal diet. The researchers measured the animals' inflammation and stress levels in the hippocampus and the prefrontal cortex in the brain after 13 weeks on the assigned diets. They compared the brains of aged mice to those of a younger set of baseline mice. The hippocampus is near the centre of the brain and is responsible for long-term memory. The prefrontal cortex, at the front of the brain, oversees complex cognitive, emotional and behavioural function.

Compared to the control group, the HFS group had significantly higher markers of inflammation, insulin resistance (altered insulin signalling) and cellular stress in areas of the hippocampus thought to be involved in the progression of Alzheimer's disease. The prefrontal cortex region of the HFS group showed more signs of insulin resistance, but inflammation and cellular stress markers did not change.

The “region specific differences between the prefrontal cortex and hippocampus in response to aging with a HFS diet [indicates] that the disease pathology is not uniform throughout the brain,” the researchers write.

The control group's inflammation levels were also increased after the trial, compared to the baseline readings. These results support the theory that aging alone plays a role in the progression of Alzheimer's disease and obesity exacerbates the effects of aging on brain function.

"This study provides novel information in relation to the mechanistic link between obesity and the transition from adulthood to middle age and signalling cascades that may be related to [Alzheimer's] pathology later in life," the research team write. "These results add to our basic understanding of the pathways involved in the early progression of Alzheimer's pathogenesis and demonstrate the negative effects of a HFS diet on both the prefrontal cortex and hippocampal regions."

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