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A Journey Through the Effects of Alzheimer’s on the Brain Part 2

Michael Mullan presents the 2nd part of : A Journey Through the Effects of Alzheimer’s on the Brain

read part 1 here

6 Signaling in the cells 

Thoughts and memories travel through nerve cells as minute electrical charges. 
One nerve cell connects to another one at synapses. As the tiny electrical charge reaches the synapse, it can release a burst of chemicals, known as neurotransmitters. The function of neurotransmitters is to carry signals to the other cells across the synapse. Scientists have discovered dozens of different neurotransmitters. 
Alzheimer’s is responsible for disrupting how electrical charges can travel while it also disrupts neurotransmitter’s activity.

Nerve Cell

 

 

7. Signal coding

With billions of nerve cells and trillions of synapses the power of the brain is sourced from numbers. Your experiences form patterns in the type of signals which explain how we are defined at a cellular level as your brain codes your memories, skills, thoughts and your sense of self. 

The scan to the left is called a positron emission tomography (PET) this shows brain activity patterns that are linked to: 

Reading of words 
Hearing words 
Thoughts about words 
Speaking words 

The red areas mark high activity levels through to the other end of the rainbow scale where yellow and violet mark low activity. 
Your patterns change over the years as you have new experiences, meet different people and learn new things. Alzheimer’s changes patterns by disrupting nerve cells and the connections between them. 

8. How Alzheimer’s Affects the Brain 

Alzheimer’s causes the brain to shrink over time, killing nerve cells and leading to tissue loss. The effects are widespread. 

A normal disease free brain 
The brain with advanced Alzheimer’s 
A comparison of the two 

Alzheimers  Brain

 

 

9. Further changes in the brain 

This is another dramatic view of the massive effects on the brain of advanced Alzheimer’s. The image is a crosswise slice of the brain. 
On the Alzheimer’s side: 
The cortex is shriveled, affecting the thought, planning and memory areas. 
The hippocampus is especially smaller than other areas, this part of the cortex controls new memory formation. 
The spaces in the brain, called ventricles, grow bigger 

10. Beneath the Microscope 

When viewed through the microscope scientists are able to see the devastating effects of the disease:

Alzheimer’s brain tissue has much less nerve cells and also synapses than a normal brain 
Build up of protein fragments called plaques occurs between the nerve cells 
The dying and dead nerve cells have tangles twisted strands made of other proteins. 

Although scientists are not certain what leads to the death of cells and loss of tissue in a brain with Alzheimer’s, the tangles and plaques are the prime suspects. 


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Reviewing New Research in Treating Alzheimer’s Disease

Synapse in brainIn a recent article discussing the findings of Korean researchers into the use of new drugs targeting Alzheimer’s disease, Lauren Horne discusses how the team may have discovered new information in the fight against the development of the disease. The study, titled “GABA from reactive astrocytes impairs memory in mouse models of Alzheimer’s disease”, is the work of Drs. Daesoo Kim and C. Justin Lee and was published in June of 2014 in the medical journal “Nature Medicine”. The article highlights how the neurotransmitter inhibitor GABA when released in higher dosages through the BESt1 channel has been shown to negatively affect the functioning of synaptic transmission, as well as plasticity, and memory. The research delves into the role that reactive astrocytes play in the development of Alzheimer’s disease, and possibly how it can be treated in the future.

According to the description of the study by Horne, the team in Korea began conducting their tests after discovering that there were large quantities of reactive astrocytes found in the brains of mice who had Alzheimer’s disease. In the course of their research, they found that the reactive astrocytes were creating the GABA transmitters through the enzyme Monoamine oxidase B(MAO-B). When the GABA transmitters were being released through the Bestrophin-1 channel, it was discovered that they were having a suppressive effect on the flow of normal information at the time of synaptic transmission.

In an attempt to reverse the effects of the B(MAO-B) that was being produced by the reactive astrocytes, the researchers utilized B(MAO-B) inhibitors to help return the levels to normal. This result of these changes was made clear in testing performed on mice with Alzheimer’s disease when their memory showed signs of improvement following the treatment. However, the benefits of the treatment using Selegiline as the inhibitor agent were not long lasting. While it has been shown to have positive results in treating Parkinson’s disease, it is unlikely that it will be use long term in treating Alzheimer’s disease.

While this study is only a preliminary entry into this avenue of research, I suspect that it holds great potential for further courses of study into finding a cure to Alzheimer’s disease.

A Fascinating Alzheimer’s Research – Sleep and Glymphatic System / Dr. Michael Mullan

images (4)What does the new study on the role of sleep in the removal of toxic waste from the brain show?

The new study from scientists at the University of Rochester has shown that sleep has a different effect on the removal of potentially toxic waste products from our brain compared to the waking state. In the rest of the body, a system called the lymphatic system removes waste accumulated from most cell types. This system, which consists of an interconnected network of tubes and lymph nodes, allows the passage of toxins in lymph back into the blood circulation. From here, most toxins from metabolic processes are destroyed in the liver or are otherwise disposed of by the body. However, the brain lacks a lymphatic system that is separate from the vasculature. Instead, cerebrospinal fluid passes from the large stores in the brain (ventricles) where it is made and passes around the arteries which provide blood to the whole brain. Much of the waste produced in the brain mixes with this cerebrospinal fluid (CSF) and passes around the outside of veins which leave the brain allowing the waste product to pass out of the brain also. This system has been called the glymphatic system and using new techniques, has now come under intense scrutiny from neuroscientists.

What is the main finding from the new study?

The new study suggests that during sleep, a much larger volume of CSF passes around the arteries and that consequently, there is a greater movement of waste products out of the brain. The researchers saw a very dramatic decrease in the influx of CSF around the arteries and into the brain when a mouse was awoken from a sleep state. Interestingly, researchers saw something similar when mice were anesthetized and therefore, unconscious. Again, there was a much greater influx of CSF around blood vessels and into the brain when the mice were unconscious. Interestingly, in order to explain why there was more CSF in the brain during sleep, the researchers showed that there was more space available to be occupied by CSF in the sleeping state. There seemed to be as much as a 60% increase in the space between brain cells during sleep allowing, the researchers suggest, more CSF to enter the brain during that time.

What is the significance of these findings for Alzheimer’s disease?

Previous studies have shown that the accumulation of the small protein amyloid in the brain is associated with damage to neurons if its accumulation goes unchecked. Previous studies have also shown that amyloid is cleared by the glymphatic system. In other words, neurons in the brain make amyloid but, these are normally taken out of the brain along the veins and harmlessly dealt with outside of the brain. The researchers showed that amyloid is cleared much more efficiently from the brain during sleep which is consistent with their findings of increased glymphatic flow during sleep. Essentially, the same finding was found during anesthesia that amyloid was cleared more rapidly from the brain. The scientists went on to show that certain brain neurotransmitters, particularly adrenaline [or norepinephrine (NE)] was responsible for reducing the amount of space available to CSF influx. They showed that by blocking receptors for adrenaline or NE, they could mimic in waking animals the increased clearance of CSF that was observed in the sleeping state.

What are the broad implications for this research for our understanding of sleep?

The reasons why all higher organisms have a need for sleep has been much debated over the centuries. It is well known that humans or animals deprived of sleep will eventually die. Fatal familial insomnia, an inherited disease caused by mutations in the prion gene leads to delirium, hallucinations, and subsequently death. Sleep may have many functions including the requirement for integration of new information acquired during the waking state. These new findings, however, suggest a more basic need for sleep (as even advanced Alzheimer cases who acquire no new memories still require sleep). The suggestion is that sleep is linked to the ability of the brain to allow additional high levels of CSF to enter and bathe the neurons and other cells in  fluid which can absorb many toxic substances including, importantly, amyloid. Future studies may look at ways to artificially manipulate the system to increase the clearance of amyloid from the brain, thus preventing its accumulation and toxic damage to neurons.

Read more about Alzheimer’s research by Michael Mullan