Vitamin B supplementation could slow the aging of neurons

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Scientists are trying to see if supplements can impact brain aging. Extreme Media/Getty Images
  • Aging can lead to cognitive decline due to changes that occur in our brain cells; however, it is unclear to what extent this is intrinsic or due to diseases such as Alzheimer’s disease.
  • In order to improve energy metabolism in the brain, a group of scientists studied the effect of supplementing a group of adults with a form of vitamin B3.
  • The researchers found that the nicotinamide riboside supplement was converted into a molecule involved in the energy metabolism of neurons.
  • They also observed a small but significant decrease in beta-amyloid protein levels in neurons after supplementation.

Age is not just a number and the mechanisms of aging affect us at the cellular level. Why some people age faster than others has been the subject of much recent research.

One condition for which age is a risk factor is dementia. About a third of people over the age of 85 have some form of dementia.

As humans live longer, the number of people with dementia in the population also increases, and the World Health Organization reports that there are currently more than 55 million people with dementia worldwide and nearly 10 million new cases each year.

Despite this high prevalence, the mechanisms and risk factors underlying dementia are poorly understood.

The prevailing understanding is that Alzheimer’s disease is thought to be underpinned by the presence of aggregates of certain forms of a protein called beta-amyloid between neurons, or nerve cells, in the brain. This is thought to affect their ability to signal, causing the cognitive decline seen in people with the condition.

However, it is important to note that there is still significant debate about this mechanism and its impact on the development of Alzheimer’s disease, as well as its suitability as a potential target for treatment.

One theory is that the decline in cognition seen in people with Alzheimer’s disease is due to disruption of typical energy production and metabolism in the brain.

A recent article published in aging cellon the topic explores whether vitamin B could help offset this disruption.

The brain is extremely dependent on energy and uses up to 20% oxygen and therefore calories, of those used by the whole body, although it is only 2% of its mass. This energy metabolism would be disturbed in the brain of people with Alzheimer’s disease.

This can be disrupted when nerve cells in the brain become insulin resistant. Insulin resistance means cells don’t use glucose for energy as they should. When this occurs in the energy metabolism of the brain, signaling and immune response functions are all negatively affected.

This can occur in people who have Type 2 diabeteswhich is characterized by insulin resistance, and there is a correlation between the disease and Alzheimer’s disease, although it is not known why.

Dr. Kellie Middleton, an orthopedic surgeon at Northside Hospital, Atlanta, Georgia, who was not involved in the study, told Medical News Today:

“Neurodegeneration is a term used to describe the progressive loss of nerve cells in the brain and spinal cord, leading to problems with memory, cognition, movement and other neurological functions. It can be caused by genetic factors or (underlying medical conditions including) aging, diabetes, stroke, Parkinson’s disease, Alzheimer’s disease or traumatic brain injury.

“Biochemical pathways are known to be associated with various forms of neurodegeneration, and research into these pathways is ongoing. For example, studies have found links between imbalances in energy metabolism, oxidative stress, inflammation and mitochondrial dysfunction with the development of neurological diseases,” she continued.

If brain cells cannot produce the energy they need to function, they cannot signal, and if nerve cells in the brain cannot signal effectively, cognition will be affected. Whether this is a cause of the disease or a symptom is unclear, said Dr. Christopher Martens, director of the Delaware Center for Cognitive Aging Research and lead author of the current study.

“One of the main challenges of Alzheimer’s disease is the disruption of energy metabolism in the brain, which may actually contribute to the development of the disease.”
— Dr. Christopher Martens

Dr. Martens and his team looked at the role of a particular molecule involved in energy metabolism, called nicotinamide adenine dinucleotide, or NAD+.

“NAD+ is essential for cells to create energy and there is strong evidence from animal studies that aging and metabolic dysfunction lead to depletion of NAD+ in cells. Therefore, there is strong evidence that the replenishment of NAD+ in the brain could have a positive effect on brain function,” he explained to DTM.

To do this, a cohort of 10 adults received a supplemental form of vitamin B3 called nicotinamide riboside, because this molecule is a precursor of NAD+. This means that the body converts it into NAD+.

A group of 12 other adults received a placebo. Neither group knew whether they were receiving the supplement or a placebo.

In order to measure whether taking 500 mg of the supplement twice a day for six weeks actually increased NAD+ in neurons, the researchers measured NAD+ in extracellular vesicles that are present in neurons and end up in the blood. They extracted them from blood samples and found a small but significant difference.

These results had already been published in 2018 in Nature.

In addition to this finding, the team has now published data showing that changes in the levels of NAD+ and its precursors correlated with changes in the presence of insulin signaling proteins and molecules involved in insulin inflammation, also thought to play a role in the development of Alzheimer’s and dementia.

While decreases in tau and amyloid proteins, thought to be implicated in the development of Alzheimer’s disease, were not significant when comparing all placebo-supplemented participants, a small but significant change was observed in levels of these marker proteins in the extracellular vesicles of a subset of supplemented participants who responded.

Still, it’s not known whether the supplement crossed the blood-brain barrier and whether these changes took place in the brain cells.

“We don’t have definitive proof that the supplement itself crosses the blood-brain barrier, especially not from our data. What we do know is that taking the supplement causes an increase in NAD+ in tiny vesicles that likely originate in the brain and other neural tissues,” Dr. Martens said. MNT.

“This is one of the big challenges in the field (d) determining if the compound can hit its target. (a) although we don’t have direct evidence, the results of our study suggest that it has a effect on the brain and also alters the metabolism of molecular pathways known to be involved in Alzheimer’s disease,” he added.

It was the next step for the team, Dr Martens said.

“This is something that we are currently actively testing in my lab in a follow-up trial in elderly people with mild cognitive impairment, but first we wanted to understand if we could detect an increase in NAD+ in the brain tissue after taking the supplement,” he added. said.

“We did this using small vesicles found in blood that we are quite sure came from neurons. What’s really interesting is that we also saw changes in more established markers of Alzheimer’s disease (eg beta-amyloid) after taking the supplement,” he added.

“Although some promising therapeutic strategies are being explored for neurodegenerative diseases, further research is needed to fully understand their potential benefits.”
—Dr. Kellie Middleton

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