High-fat diet causes the connections between neurons to be degraded

Consuming a high-fat diet causes most living organisms to become obese, but apparently, another bad effect of having a high-fat diet includes causing the normally busy immune cells in our brain to become inactive and start eating up the connections between our neurons.

Fortunately, going on a low-fat diet for just two months apparently reverses the effect of having lowered
cognitive ability as weight begins to go back to normal, at least in mice.

Microglia eating synapses is contributing to synapse loss and cognitive impairment in obesity, said Dr.
Alexis M. Stranahan, neuroscientist in the Department of Neuroscience and Regenerative Medicine at the
Medical College of Georgia, and the corresponding author of the study published in the journal Brain,
Behavior, and Immunity. On the one hand, that is very scary, but it's also reversible, meaning that if you
go back on a low-fat diet that does not even completely wipe out the adiposity, you can completely
reverse these cellular processes in the brain and maintain cognition.

What happens is that when the body accumulates too much fat, the microglia in the brain initiate an
autoimmune response. Microglia have the same ability as macrophages, in which they are able to ingest
waste and other harmful materials in the brain, which supposedly supports the function and maintains
the health of neurons. However, when the mice get obese, the microglia seem to overeat.

High Fat Diet and Neurons

The study used male mice in which one group was given a diet that consisted of chow that had 10 percent
of the calories coming from saturated fat, while the other group had 60 percent. The researchers also
made sure that both chows were similar in other key ingredients. In human terms, it was like having a
healthy diet versus a fast-food diet.

At four, eight and twelve weeks, the scientists measured metabolic indicators, such as weight, food intake,
insulin and serum glucose levels. At the same time, they also measured the levels of proteins that
indicated the number of synapses in the hippocampus, which is the center of learning and memory.

At four weeks, levels in both groups of mice were the same. At eight weeks, everything was also pretty
much the same except for weight, in which mice who were on the high-fat diet were fatter. At twelve
weeks, the mice on a high-fat diet were obese, had elevated cytokine levels and had a reduced number
of synapse markers and function.

After twelve weeks, the researchers change half of the mice having the high-fat diet to a low-fat diet, and
it took around 2 months for their weight to go back to normal. On the other hand, those who were still
on a high-fat diet continued to get fat, getting more inflamed and lost more synapses. The microglial
structures called processes, which normally help in maintaining synaptic function, continued to weaken.
Similarly, dendritic spines on neurons which get input from synapses also withered with the high-fat diet.
However, converting to the low-fat diet both components of both cells were restored.

Obesity causes extreme overkill in microglial cells, which are usually sensitive and very crucial in
maintaining the health of neurons. This is very promising, said Stanahan. The results that were seen in
the study could open new purposes for drugs used for conditions such as rheumatoid arthritis and Crohn's
disease, which block inflammatory cytokines, which are elevated in the brains of obese mice.