Hello everyone and welcome to this week's article, where I will be exploring the various recent advances in dementia research. For an introduction to what dementia is, make sure you read part one of my article here.
Using walking patterns to diagnose dementia
In September 2019, researchers at the University of Newcastle attempted to show that the walking patterns of people with Alzheimer's are slightly different than those suffering from Lewy body dementia. To do this, they set up a walkway paved with thousands of sensors to capture participants footsteps as they walked across it. This experiment proved that their walking patterns are in fact different - people with Lewy body dementia frequently changed their stride length and the time it took them to make each step, whereas people with Alzheimer's disease walked consistently.
This is important for medicine as it provides another clear way in which these forms of dementia can be diagnosed and be differentiated from each other, without needing invasive diagnostic tests. As such, a more accurate diagnosis can be made in less time, meaning that patients can receive specific treatment and care for the type of dementia they have earlier.
The use of antibiotics in frontotemporal dementia treatment
Frontotemporal dementia is a type of dementia that results from the deterioration of the frontal and temporal lobe. It is the second most common form of dementia and typically results in mood swings, memory loss and speech difficulty.
According to researchers, a subgroup of frontotemporal dementia sufferers' have a genetic mutation which stops the brain producing a specific protein called progranulin. While the impact of the absence of this protein is not yet known, the study's authors believe that it likely contributes to the disease.
Nevertheless, the brain can be tricked into producing this protein by adding antibiotic molecules to the affected cells. Although the aminoglycoside antibiotic molecules gentamicin B1 and G418 were both able to increase the production of progranulin, researchers concluded that the G418 molecules were more effective in doing so.
Hopefully, by continuing research in this area, we could develop a medication that can cure this form of dementia. Nonetheless, it should be stressed that this research is only in its early stages and we are still many years away from developing such medication. Furthermore, not only does the use of these antibiotics come with many negative side effects, but it is still not known whether increasing the production of progranulin in sufferers of frontotemporal dementia would actually have a positive effect.
Is a vaccine for dementia possible?
As you will recall from part 1 of my article, Alzheimer's disease, which is the most common form of dementia, is caused by the accumulation of beta-amyloid plaques and tangles of tau in the brain. The build-up proteins then cause the symptoms associated with Alzheimer's disease, such as memory loss and cognitive decline.
Dementia affects over 50 million people across the world and this number is expected to double every 20 years, rising to 131.5 million in 2050. As such, due to the huge impact dementia has on our society both socially and economically, there is a lot of pressure on scientists to develop a cure or vaccine for the disease.
A large amount of research has been done in developing a cure for the disease, however, to date no medications have been proven successful in human trials, Research published at the end of 2019 shows some promise though and, with more research, may culminate in the development of a vaccine. Earlier studies have shown that the two vaccines AV-1959R and AV-1980R both induced an antibody response to the plaques and tangles in the brain caused by dementia.
By using mice studies, researchers at Flinders University in Australia then built on this research to explore what would happen if both vaccines were delivered at the same time, along with an adjuvant (a substance that modifies the effect of other agents) called AdvaxCpG. What they found was that the combined therapy dramatically increased the production of antibodies to tau and beta-amyloid, which in turn assisted in the reduction of the number of plaques and tangles. Furthermore, they also discovered that the adjuvant AdvaxCpG helped strengthen the immune response induced by this experimental vaccine.
New research into stopping a toxic protein buildup in Parkinson's disease
Parkinson's disease is a form of dementia which affects over 10 million people across the globe. The symptoms of Parkinson's include involuntary shaking, slow movement, stiffness of muscles and balance problems.
Parkinson's disease is caused by the buildup of a misfolded protein called alpha-synuclein. This then leads to the loss of nerve cells in the substantia nigra (a part of the brain), resulting in a reduction of dopamine release. This reduction of dopamine is what culminates in the symptoms of Parkinson's.
Researchers in the United States have managed to utilise new technology to develop a compound which blocks the synthesis of this faulty protein. This compound, which they called Synucleozid, targets the mRNA which codes for this protein, preventing gene expression. This research could prove vital in increasing the quality of life of Parkinson's disease as, by reducing the build-up of alpha-synuclein, the progression of the disease can be drastically slowed down. Moreover, this compound could also be used in sufferers of Lewy body dementia, as the presence of alpha-synuclein is also significant in that disease. Nonetheless, one must stress that this research is in its very early stages, and we are still years before Synucleozid can be used in treatment.
I hope you enjoyed this week's article, which outlined the latest research into dementia. Make sure to subscribe to the mailing list below so that you get notified when the next article is released!
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