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Aging Brain and Mental Performance

Stem Cells in the Brain Control Aging Speed

4 months, 3 weeks ago

3955  0
Posted on Jul 27, 2017, 5 p.m.

Researchers have discovered that stem cells in the brain's hypothalamus control how fast aging occurs in the body.  

Albert Einstein College of Medicine scientists have determined that stem cells produced in the brain's hypothalamus dictate the speed at which body aging occurs. The finding was made through an in-depth study of mice. There is hope that this breakthrough will pave the way for new strategies that delay or prevent diseases related to the aging process. The end result could be a significant increase in lifespan. The details of the findings were recently published in Nature.

About the Finding

Scientists have long known that the hypothalamus regulates vital processes like reproduction, growth, development, and metabolism. Three years ago Einstein College of Medicine academicians made the surprising finding that the hypothalamus regulates aging throughout the entirety of the body. The scientists have now identified the hypothalamus cells that regulate the aging process. They are a small group of adult neural stem cells that were previously known to be central to the formation of new neurons within the brain.

The research shows the amount of hypothalamic neural stem cells gradually declines across the animal's life. This decline speeds up the aging process. It was also determined the effects of the loss can be reversed. A replenishing of the stem cells or the molecules they generate can slow or even reverse aging in the body.

To determine whether stem cells within the hypothalamus were important to the aging process, the research team examined the fate of those specific cells as healthy mice aged. The number of hypothalamic stem cells started to decrease when the animals hit the 10-month mark. This is several months ahead of the point when the typical signs of aging begin to manifest.

By the period of old age for mice (about two years old), the majority of the cells were gone. The research team examined what occurred when selectively disrupting middle-aged mice's hypothalamic stem cells to determine if the gradual loss of stem cells was responsible for aging. The disruption dramatically accelerated the aging process compared to mice in the control group. Mice with disrupted stem cells perished earlier than those in the control group.

The researchers applied hypothalamic stem cells to the brains of middle-aged mice in which stem cells were destroyed. They also injected stem cells into the brains of regular old mice. Both groups exhibited a slowing or complete reversal of aging measures.

How the Process Works

The research team determined hypothalamic stem cells produce anti-aging effects with the release of chemicals referred to as microRNAs. They are not a component of protein synthesis yet they play important roles in regulating gene expression. MicroRNAs are packaged within diminutive particles referred to as exosomes that the hypothalamic stem cells send out into cerebrospinal fluid.

The research team extracted exosomes containing microRNAs from hypothalamic stem cells and inserted them in the cerebrospinal fluid of two different mice groups: regular middle-aged mice and middle-aged mice in which hypothalamic stem cells were destroyed.

The treatment dramatically slowed the aging process in each group. This determination was made through behavioral testing as well as tissue analysis. Such measurements assessed alterations in the animals' cognitive abilities, muscle endurance, social behavior, and coordination.

What's Next?

The research team is now attempting to pinpoint specific populations of microRNAs and other factors stem cells secrete that produce anti-aging effects. This is an important step toward the end goal of slowing the aging process and treating diseases related to aging.

Yalin Zhang, Min Soo Kim, Baosen Jia, Jingqi Yan, Juan Pablo Zuniga-Hertz, Cheng Han, Dongsheng Cai. Hypothalamic stem cells control ageing speed partly through exosomal miRNAs. Nature, 2017; DOI: 10.1038/nature23282

https://www.sciencedaily.com/releases/2017/07/170726132107.htm

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