Hold the Fries: High Fat Diet Exacerbates Cognitive Decline in a Mouse Model of Alzheimer's
Article Highlights:
- Chronic, high fat diet led to:
- An increase in deposition of amyloid plaques - aggregates of protein that are seen in the brains of Alzheimer's patients.
- Decreased activity of genes involved with building connections and sending signals between neurons
- Increased activity of genes involved with inflammation and immune system activity
- Decreases is cognitive performance compared to mice fed a normal diet.
Summary:
Studying a mouse model of Alzheimer's, scientists at the University of Pittsburgh found that a high-fat diet exacerbated the condition. Nam et al. have published their open-access findings in Scientific Reports. In their study, mice were fed a diet composed of 40% fat, over twice as much compared to mice fed a normal diet (16% fat). The high fat diet mice performed worse in escaping a maze designed to study the ability to form memories. The mice also had increased plaque deposition in the brain, and lower expression of key genes which are related to the maintenance and development of the nervous system, memory formation, and overall number of neurons. There was also an increase in genes associated with inflammation and apoptosis, which is a regulated form of cell death.
Interestingly, mice on a high fat diet also had changes in the composition of fatty molecules in their brains - a group of molecules collectively called "the lipidome." These fatty molecules make up cell membranes, have roles in cell-signaling, and can cause impairments in the metabolic function of cells. Changes in the composition of these compounds likely has a large number of effects on the brain.
Discussion:
This is the second mouse model of Alzheimer's these researches have tested with a high fat diet. In both model systems, the high fat diet group fared worse overall in cognition and accumulation of protein plaques. Although interesting, and perhaps significant, these findings have yet to be duplicated in humans. These mouse models used here have specific mutations which cause them to develop an Alzheimer's-like condition. In humans, the disease is often far more complex, and the way to body responds to a high fat diet may indeed be different. It does warrant further studies, however, to determine if a diet high in fat may quicken the progression of Alzheimer's disease, and importantly, whether it may contribute to the initial development of the condition.
References
Nam K.N.,et al. Effects of high fat diet on phenotype, brain transcriptome and lipidome in Alzheimer's model mice. Scientific Reports. 2017, (7): 4307. Epub ahead of print.
Fitz, N. F. et al. Liver X receptor agonist treatment ameliorates amyloid pathology and memory deficits caused by high-fat diet in APP23 mice. The Journal of Neuroscience: The Official Journal of the Society for Neuroscience (30) 6862–6872