A protein in your brain can be your weapon against Alzheimer’s disease

Researchers have found that a protein that regulates white blood cells in the human brain could protect against Alzheimer’s disease.

The results  suggest that this protein, called CD33, could have important implications in the fight against Alzheimer’s disease.

“Immune cells in the brain, called microglia, play a critical role in Alzheimer’s disease,” explained  co-author of the study.

“They can be harmful or protective. Swaying microglia from a harmful to protective state could be the key to treating the disease,” the author added. Scientists have identified the CD33 protein as a factor that may decrease a person’s likelihood of this disease.

Now, this research has shown that the most common type of CD33 protein plays a crucial role in modulating the function of microglia. “The fact that CD33 is found on microglia suggests that immune cells can protect the brain from Alzheimer’s disease under the right circumstances,” said the  first author of the study.

Alzheimer’s disease affects more than 44 million people around the world. “These findings set the stage for future testing of a causal relationship between CD33 and Alzheimer’s Disease, as well as testing therapeutic strategies to sway microglia from harmful to protecting against the disease – by targeting CD33,” said the researcher.

“Microglia have the potential to ‘clean up’ the neurodegenerative plaques, through a process called phagocytosis — so a therapy to harness this ability to slow down or reverse this mental health disorder can be envisioned,” he said.


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The Brain Literally Starts Eating Itself When It Doesn't Get Enough Sleep

The reason we sleep goes far beyond simply replenishing our energy levels every 12 hours - our brains actually change states when we sleep to clear away the toxic byproducts of neural activity left behind during the day.

Weirdly enough, the same process starts to occur in brains that are chronically sleep-deprived too - except it's kicked into hyperdrive. Researchers have found that persistently poor sleep causes the brain to clear a significant amount of neurons and synaptic connections, and recovering sleep might not be able to reverse the damage.

A team led by neuroscientist Michele Bellesi from the Marche Polytechnic University in Italy has examined the mammalian brain's response to poor sleeping habits, and found a bizarre similarity between the well-rested and sleepless mice.

Like the cells elsewhere in your body, the neurons in your brain are being constantly refreshed by two different types of glial cell- support cells that are often called the glue of the nervous system.

The microglial cells are responsible for clearing out old and worn out cells via a process called phagocytosis  - meaning "to devour" in Greek.

The astrocytes' job is to prune unnecessary synapses (connections) in the brain to refresh and reshape its wiring. 

We've known that this process occurs when we sleep to clear away the neurological wear and tear of the day, but now it appears that the same thing happens when we start to lose sleep.
But rather than being a good thing, the brain goes overboard with the clearing, and starts to harm itself instead.

Think of it like the garbage being cleared out while you're asleep, versus someone coming into your house after several sleepless nights and indiscriminately tossing out your television, fridge, and family dog.

"We show for the first time that portions of synapses are literally eaten by astrocytes because of sleep loss," Bellesi told Andy Coghlan at New Scientist.

To figure this out, the researchers imaged the brains of four groups of mice:

• one group was left to sleep for 6 to 8 hours (well-rested)
• another was periodically woken up from sleep (spontaneously awake)
• a third group was kept awake for an extra 8 hours (sleep-deprived)
• and a final group was kept awake for five days straight (chronically sleep-deprived).

When the researchers compared the activity of the astrocytes across the four groups, they identified it in 5.7 percent of the synapses in the well-rested mouse brains, and 7.3 of the spontaneously awake mouse brains.
In the sleep-deprived and chronically sleep-deprived mice, they noticed something different: the astrocytes had increased their activity to actually eating parts of the synapses like microglial cells eat waste - a process known as astrocytic phagocytosis. 

In the sleep-deprived mouse brains, the astrocytes were found to be active across 8.4 percent of the synapses, and in the chronically sleep-deprived mice, a whopping 13.5 percent of their synapses showed astrocyte activity.

As Bellesi told New Scientist, most of the synapses that were getting eaten in the two groups of sleep-deprived mice were the largest ones, which tend to be the oldest and most heavily used - "like old pieces of furniture" - which is probably a good thing.

But when the team checked the activity of the microglial cells across the four groups, they found that it had also ramped up in the chronically sleep-deprived group.

And that's a worry, because unbridled microglial activity has been linked to brain diseases like Alzheimer's and other forms of neurodegeneration.

"We find that astrocytic phagocytosis, mainly of presynaptic elements in large synapses, occurs after both acute and chronic sleep loss, but not after spontaneous wake, suggesting that it may promote the housekeeping and recycling of worn components of heavily used, strong synapses," the researchers report.

"By contrast, only chronic sleep loss activates microglia cells and promotes their phagocytic activity ... suggesting that extended sleep disruption may prime microglia and perhaps predispose the brain to other forms of insult."

Many questions remain, such as if this process is replicated in human brains, and if catching up on sleep can reverse the damage.

But the fact that Alzheimer's deaths have increased by an incredible 50 percent since 1999, together with the struggle that many of us have in getting good night's sleep means this is something we need to get to the bottom of - and fast.

The research has been published in the Journal of Neuroscience.

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Skin cells help activate hair re-growth

A new study has provided a deeper insight into how to activate hair re-growth with the help of skin cells.

A group from the Spanish National Cancer Research Centre (CNIO) has discovered an unexpected link between the body's defense system and skin regeneration. It turns out that macrophages are involved. These are cells from the immune system that are in charge of devouring invading pathogens, a process called phagocytosis.

The authors report that macrophages induce hair growth by surrounding and activating cells in the skin that have regenerative capacity, called stem cells. The discovery that macrophages activate skin stem cells could influence technologies with potential applications in tissue regeneration, aging, and cancer.

Donatello Castellana, from the Epithelial Cell Biology Group of the BBVA Foundation-CNIO Cancer Cell Biology Programme, said that the researchers used tiny droplets, or liposomes, to carry the drug used in the study. The future use of liposomes as a way to deliver a drug to specific cells looks promising and might have additional implications for the study of several pathologies.

The study is published in the journal PLOS Biology. 


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