Alzheimer’s Disease: Can we cure the confusion?

Science, Technology 2015-06-11

So, June is Alzheimer’s and Brain Awareness Month and with the disease affecting 520000 people in the UK alone, I thought it would be perfect to dedicate a blog post to the condition. Alzheimer’s impacts millions of us worldwide, not only those struggling with the disease but also their family members and caregivers. It is time to put a stop to Alzheimer’s, cure the confusion and preserve our memories.

What is Alzheimer’s Disease?

Alzheimer’s is a progressive, degenerative brain disease and is the most common cause of dementia; a group of brain disorders affecting a person’s memory, thinking and the ability to interact socially. The brains of Alzheimer’s patients show two characteristic features: plaques and tangles. Plaques are formed from lots of sticky proteins called beta amyloid whilst tangles are made up from twisted strands of a protein called tau. These proteins build up in the brain and become toxic, damaging nerve cells and ultimately causing brain shrinkage and memory loss.

 

The disease doesn’t just arouse confusion in its patients but also amongst scientists. With very little known about it, scientific discoveries are of exceptional significance in both our understanding of the disease and in the development of treatment. There are currently no treatments available to reverse or stop the progression of Alzheimer’s, but there have been four notable breakthroughs in 2015 so far that give us great hope that soon this will all be about to change.

 

Alzheimer’s Disease Potential Treatments

A landmark study on mice, carried out by Professor Christian Hölscher of the University of Lancaster, found that the diabetes drug Liraglutide reduced the damage caused by Alzheimer’s and resulted in memory improvements. Mice with late stageAlzheimer’s that were treated with the drug performed significantly better on object recognition tests and their brains showed a 30% reduction in the build up of amyloid plaques.

So how does Liraglutide work? It activates receptors on neurons that initiate a growth-factor type signalling cascade in motion. The result of this is that the cell repair of neurons is improved, the energy metabolism is normalised and synapses are maintained. This reduces the oxidative stress and so growth and replacement of neurons is enhanced. Overall the brain is in a much better position to deal with stress and toxic influences.

A new study led by Imperial College London is recruiting over 200 patients, aged 50 and over with the early onset of Alzheimer’s disease, to a year-long human trial for the drug which will involve brain scans and memory function tests. If the study is successful, Liraglutide would become the first treatment to reverse the progression of Alzheimer’s and it would herald the most significant breakthrough in over 30 years.

 

Potential Drug Targets for Alzheimer’s Disease 

The pathogenesis of Alzheimer’s and what causes neuronal dysfunction is the question numerous scientists are pondering. A study by Duke University has begun to answer this very question.

Duke University’s new study in mice indicates that the amino acid arginine is important in the progression of Alzheimer’s disease.

The research team studied immune cells called microglia in mice bred to develop Alzheimer’s disease. These mice were observed to have higher numbers of microglia in their brains compared to normal mice. Microglia normally play a protective role in the immune system, scanning the central nervous system for plaques, damaged neurons and infectious agents. However research suggests that they switch to become more harmful during the course of the disease.

Microglia express a molecule, CD11c, on their surface and in the study these cells were isolated and their patterns of gene activity were analysed. The research team found that the genes that usually fired up the immune system were now having the opposite effect and were dampening the immune response. They also saw heightened expression of genes involved in immune suppression. The group found that CD11c microglia and arginase, an enzyme that breaks down arginine, were highly expressed in regions of the brain associated with memory. The lower levels of arginine are thought to contribute to the death of nerve cells and subsequently neurodegenaration.

Mice were treated with a chemical that blocks the breakdown of arginine, difluoromethylornithine (DFMO) before the onset of symptoms. Scientists saw fewer CD11c microglia and fewer Alzheimer’s plaques in the brains of mice. Furthermore mice that were treated with DMFO performed better on memory tests than the untreated mice did.

The study suggests that if you block the process of arginine deprivation then the mouse can be protected from Alzheimer’s. It is not as simple as consuming more arginine through the diet as blood vessels determine how much arginine can enter the brain. Furthermore unless blocked, arginase would still break down arginine, so DMFO seems like the perfect solution. DMFO is currently being investigated in human clinical trials for cancer and is yet to be tested as potential therapy of Alzheimer’s.

 

A Drugs-Free Approach to AD

The association between Alzheimer’s and the accumulation of plaques is very well known, is there a non-invasive treatment that might be able to remove these toxic plaques?

A study carried out by researchers from the University of Queensland, Australia, have found that ultrasound successfully breaks apart the neurotoxic amyloid plaques from the brains of mice – these are the structures thought to  be responsible for memory loss and decline of cognitive function in Alzheimer’s patients.

The ultrasound waves oscillate extremely quickly, activating microglial cells that digest and remove the amyloid plaques that are destroying brain synapses, and in doing so improve memory and cognitive function.

It may take several years before this innovative drugs-free approach goes to human trials, but when it does the results could be profound.

 

An Opportunity for New Research

A recent discovery by the University of Virginia Health System could have profound implications for the study and treatment of neurological disorders including Alzheimer’s. Researchers have determined that the brain is directly connected with the immune system through lymphatic vessels that were not previously known to exist. It is suggested that these vessels are very likely to play a key role in neurological diseases that have an immune component to them.

 

Hope for the future

Vast improvements in healthcare over the last 100 years have contributed to people having much longer life expectancies. Subsequently this has also resulted in an increase in the number of people living with dementia.

Alzheimer’s predominantly affects those 65 and older.

Nearly 44 million people suffer with Alzheimer’s, worldwide. By 2030 if breakthroughs are not discovered, we will see this number escalate to nearly 76 million. Every four seconds, a new case of dementia occurs somewhere in the world. This emphasises the significance of the current scientific breakthroughs described in this blog and the importance of research to continue moving forward, closer to the cure of this devastating disease.

A common theme that connects the breakthroughs mentioned is that the immune system, which usually protects us from disease and other damaging bodies, plays a part in Alzheimer’s disease. However, the exact role of the immune system is still unknown. Research into the lymphatic vessels connecting the brain to the immune system could provide us with some much-needed answers.

All in all, this gives us hope that the number of sufferers can be greatly reduced. Continued research will enable us to increase our understanding of the disease and develop treatments. Let’s cure the confusion.

 

Got something to say about #Alzheimer’s? Tweet me @HannahAtNotch

 

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