Lifeboat Foundation

A new study is suggesting a metabolite produced by gut microbes could increase neuron production in the brain, improve intestinal function, and ultimately slow the aging process. Across several compelling mouse experiments the research found the negative effects of aging could be counteracted by enhanced microbial production of a molecule called butyrate.

Investigating the effect of the gut microbiome on aging, the new research first performed gut microbiome transplants between old and young mice. Using fecal transplants, young germ-free mice were colonized with the gut microbiota of older mice. The results were somewhat unexpected as the younger mice colonized with the older microbiomes displayed increased neurogenesis, a process whereby new neurons are produced in the brain.

“We’ve found that microbes collected from an old mouse have the capacity to support neural growth in a younger mouse,” explains Sven Pettersson, lead on the research team from Nanyang Technological University in Singapore. “This is a surprising and very interesting observation…”

The evolution of human diets led to preferences toward polyunsaturated fatty acid (PUFA) content with ‘Western’ diets enriched in ω-6 PUFAs. Mounting evidence points to ω-6 PUFA excess limiting metabolic and cognitive processes that define longevity in humans. When chosen during pregnancy, ω-6 PUFA-enriched ‘Western’ diets can reprogram maternal bodily metabolism with maternal nutrient supply precipitating the body-wide imprinting of molecular and cellular adaptations at the level of long-range intercellular signaling networks in the unborn fetus. Even though unfavorable neurological outcomes are amongst the most common complications of intrauterine ω-6 PUFA excess, cellular underpinnings of life-long modifications to brain architecture remain unknown. Here, we show that nutritional ω-6 PUFA-derived endocannabinoids desensitize CB1 cannabinoid receptors, thus inducing epigenetic repression of transcriptional regulatory networks controlling neuronal differentiation. We found that cortical neurons lose their positional identity and axonal selectivity when mouse fetuses are exposed to excess ω-6 PUFAs in utero. Conversion of ω-6 PUFAs into endocannabinoids disrupted the temporal precision of signaling at neuronal CB1 cannabinoid receptors, chiefly deregulating Stat3-dependent transcriptional cascades otherwise required to execute neuronal differentiation programs. Global proteomics identified the immunoglobulin family of cell adhesion molecules (IgCAMs) as direct substrates, with DNA methylation and chromatin accessibility profiling uncovering epigenetic reprogramming at 1400 sites in neurons after prolonged cannabinoid exposure. We found anxiety and depression-like behavioral traits to manifest in adult offspring, which is consistent with genetic models of reduced IgCAM expression, to suggest causality for cortical wiring defects. Overall, our data uncover a regulatory mechanism whose disruption by maternal food choices could limit an offspring’s brain function for life.

• Immediate Communication
• Published: 18 November 2019

• Valentina Cinquina ¹,
• Daniela Calvigioni ¹,
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It seems incredible that scientists have discovered a new human organ. I mean, they cut people open right and left (living and dead). How could they miss anything?

Well, they did. A new organ has been identified. Actually, two. Plus a new “structure” that is not quite an organ.

First, the “structure”: In 2017, an elaborate system of drainage vessels was seen in the brain for the first time. Until then their existence was suspected, but not certain.

Transplanting embryonic progenitor interneurons into the hippocampus of mouse models of TBI, researchers noticed the neurons migrated to the injury site and made new connections. Following treatment, memory improved and seizures were reduced.

Did you know that obesity, autoimmune disease, diabetes, arthritis, depression, anxiety and eczema all have one thing in common? It’s the gut.

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New finding sheds new light on how the brain processes spatial memory.

Summary: Inflammation appears to have a negative impact on attention and cognition. Source: University of BirminghamScientists at the University of Birmingham in collaboration with the Universi.

Think about it. Your brain is always “on.” It takes care of your thoughts and movements, your breathing and heartbeat, your senses — it works hard 24/7, even while you’re asleep. This means your brain requires a constant supply of fuel. That “fuel” comes from the foods you eat — and what’s in that fuel makes all the difference. Put simply, what you eat directly affects the structure and function of your brain and, ultimately, your mood.

Like an expensive car, your brain functions best when it gets only premium fuel. Eating high-quality foods that contain lots of vitamins, minerals, and antioxidants nourishes the brain and protects it from oxidative stress — the “waste” (free radicals) produced when the body uses oxygen, which can damage cells.

Unfortunately, just like an expensive car, your brain can be damaged if you ingest anything other than premium fuel. If substances from “low-premium” fuel (such as what you get from processed or refined foods) get to the brain, it has little ability to get rid of them. Diets high in refined sugars, for example, are harmful to the brain. In addition to worsening your body’s regulation of insulin, they also promote inflammation and oxidative stress. Multiple studies have found a correlation between a diet high in refined sugars and impaired brain function — and even a worsening of symptoms of mood disorders, such as depression.