29 Jun 2018 --- When a high-fat, high-sugar (HFS) diet that leads to obesity is paired with normal aging, it may contribute to the development of Alzheimer’s disease, finds a study published in Physiological Reports. Also, researchers discovered that certain areas of the brain respond differently to risk factors associated with Alzheimer's, indicating that the pathology is not uniform throughout the brain.
“This study provides novel information in relation to the mechanistic link between obesity and the transition from adulthood to middle age and signaling cascades that may be related to [Alzheimer's] pathology later in life,” say the researchers. “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 high fat, high sugar diet on both the prefrontal cortex and hippocampal regions.”
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 the development of the disease.
Researchers from Brock University in Ontario, Canada, looked at the effects of an obesity-inducing diet on insulin signaling (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, 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 center of the brain and is responsible for long-term memory. The prefrontal cortex, at the front of the brain, oversees complex cognitive, emotional and behavioral function.
Compared to the control group, the HFS group had significantly higher markers of inflammation, insulin resistance (altered insulin signaling) 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 wrote.
The control group's inflammation levels were also increased after the trial when 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.
NutritionInsight has reported widely on the effects diet can have on brain health and degenerative brain disease. A study published in the journal Brain, Behavior, and Immunity found that adolescent rats who consumed a diet high in saturated fats are at an increased risk of psychopathology in adulthood and the subjects began exhibiting behaviors that mirror post-traumatic stress disorder (PTSD). A common protein found in species of fish, parvalbumin, was found to perhaps prevent the formation of specific protein structures that are closely associated with Parkinson’s disease, a Swedish study discovered. The Chalmers researchers discovered that parvalbumin can form amyloid structures that bind together with the alpha-synuclein protein. Parvalbumin effectively “scavenges” the alpha-synuclein proteins, using them for its own purposes, thus preventing them from forming their own potentially harmful amyloids at a later point.
Furthermore, strengthening the age-old saying, “we are what we eat,” research has detailed that following a low-fat diet in combination with limited caloric consumption could prevent age-related brain dysfunction.
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