Posts Tagged ‘Astrocyte’

The Brain Starts to Eat Itself After Chronic Sleep Deprivation

June 30, 2017

The title of this post is identical to the title of an article by Andy Coghlan in the News & Technology section of the May 27, 2017 issue of the New Scientist. Michele Belles of the Marche Polytechnic University in Italy says the chronic sleep deprivation could explain why a chronic lack of sleep puts people at his age of Alzheimer’s disease and other neurological disorders.

The brain cells that destroy and digest worn-out cells and debris go into overdrive in mice that are chronically sleep deprived. Although this might b beneficial in the short term, clearing potentially harmful debris and rebuilding worn circuitry might protect health connections. But when this continues in the long term it destroys healthy brain material.

The researchers specifically looked at glial cells, which serve as the brain’s housekeeping system. Previous research had found that a gene that regulates the activity of these cells is more active after a period of sleep deprivation. One type pf glial cell called an astrocyte, removes unnecessary synapses in the brain to remodel its wiring. Another type of cell, called a microglial cell, prowls the brain for damaged cells and debris.

The research suggest that sleep loss can trigger astrocytes to start breaking down more of the brain’s connections and their debris. Bells says, “We show for the first time that portions of synapses are literally eaten by astrocytes because of sleep loss.

The researcher found that microglial cells were more active after chronic sleep deprivation (Journal of Neuroscience, 10.1523/JNEUROSCI.3981-16.2017). Excessive microglial activity has been linked to a range of brain disorders. Bells says, “We already know that sustained microglial activation has been observed in Alzheimer’s and other forms of neurodegeneration.

This research could explain why a lack of sleep seems to make people more vulnerable to developing such dementias.

It is still not clear whether getting more sleep could protect the brain or rescue if from the effects of a few sleepless nights. The researchers plan to investigate how long the effects of sleep deprivation last.

To learn more about the effects of sleep deprivation, enter “sleep deprivation” into the search block of the healthymemory blog.dem



Astrocytes and Alzheimer’s

October 14, 2012

Astrocytes are star shaped glial cells found in the brain and the spinal cord. An interesting article1 explains how these astrocytes could possibly prevent or provide a cure for Alzheimer’s. It is thought that these astrocytes make up a large percentage of the brain and have an important role supporting neurons to include clearing the beta-amyloid plaques associated with Alzheimer’s. It was recently shown that cells in the brains of people with Alzheimer’s “senesce.” This mechanism stops them from dividing and starts them on a path of destruction.

It is generally believed that cell senescence evolved to protect us from cancer. Cells can accumulate DNA damage as they age and they senesce to avoid incorrect division that can lead to cancer. The benefit of senescence over self-destruction is that it sends out a call to the immune system to destroy nearby cells that might also be affected. If the damaged cell is not killed, it goes on pumping out inflammatory proteins, which can cause damage thought to underlie age related ailments such as Alzheimer’s.

To provide some empirical data, brain slices were taken from cadavers. Slices were taken from fetuses, from people aged 35 to 50, and from people aged between 78 and 90.  The healthy brains from adults over 35 had six to eight times more senescent cells than those taken from fetuses. Cells from corpses who had had Alzheimer’s had more of these cells than their Alzheimer-free pairs of similar age. About 30 percent of the of the astrocytes seem to have senesced, a figure that was 10 percent higher in those with Alzheimer’s.

The theory is that the plaques and aging astrocytes get caught in a vicious cycle.  As the astrocytes senesce, they are less able to perform their plaque cleaning duties, and the accumulation of plaques drives more cells to senesce.2 If the astrocytes could be kept young, they could clear the plaque. The problem with preventing senescence is that it could increase the risk of cancer. Another approach is to get rid of the senescent cells. Research using mice has found that a technique for removing all of the senescent cells in a mouse prevented the onset of a range of age-related disorders. If this technique can be adapted for humans and the senescent cells can be cleared, then Alzheimer;s could probably be cleared.

Another approach might be to stop senescing brain cells from secreting their inflammatory brew. They have been found a compound that suppresses the secretions of senescent cells in the laboratory. That needs to be transitioned and tested with humans.

This work is quite promising. However, it should be remembered that beta-amyloid plaque might be a necessary condition, but it is not a sufficient condition for the onset of Alzheimer’s. There have been autopsies done of individuals whose brains were plagued by beta-amyloid plaque who had never shown any of the symptoms of Alzheimer’s when they were alive.

It is thought that keeping cognitively and physically active, and continuing to grow cognitively as we age builds up a cognitive reserve that resists or offsets these physical symptoms.

1Hamzelou, J. (2012). Why Alzheimer’s Hits Older Brains. New Scientist, 29 September, 6-7.

2Bhat, R., Crowe, E.P., Bitto, A. , Moh, M., Katsetos, C.D., Garcia, F.U., Johnson, F.B., Trojanski, J.Q., Sell, C., Torres, C. (2012). Astrocyte Senescence as a Component of Alzheimer;s Disease. PloS,

© Douglas Griffith and, 2012. Unauthorized use and/or duplication of this material without express and written permission from this blog’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to Douglas Griffith and with appropriate and specific direction to the original content.