Post by alice on Aug 6, 2017 10:22:51 GMT -5
Alzheimer’s Society website
Friday 7 April 2017
Finding the common ground between Alzheimer’s and Parkinson’s at the ADPD conference
Dr Clare Walton from our research team has just returned from the Alzheimer’s and Parkinson’s disease Congress (also known as ADPD), which was held in Vienna from 29 March to 2 April 2017. Here she reflects on the latest research she saw there.
Timeline of landmark discoveries in Alzheimer’s disease at ADPD. Photo credit: @thegblab on Twitter
The Alzheimer’s and Parkinson’s Disease (ADPD) Congress happens every two years. It brings together over 3,000 researchers from the field of neurodegeneration. This includes specialists in Alzheimer’s and Parkinson’s diseases but also on Parkinson’s disease dementia, Lewy body dementia, frontotemporal dementia and some other rarer conditions. From a clinical perspective, bringing these research fields together to share their latest findings makes a lot of sense. Although we define each of these forms of dementia as different conditions, we are increasingly learning that there is overlap between them.
Learning from each other
Several speakers, including Dr Lauren Walker from the University of Newcastle, reported that it is common to find that people have the biological hallmarks of more than one type of dementia in their brain. These hallmarks can be seen in a person’s brain tissue after they have died and, more recently, also in living people using innovative new brain imaging techniques.
Perhaps unsurprisingly, people who show signs of more than one type of dementia experience faster declines in cognitive function. These findings have important implications for the treatment of people with dementia. For example toxic clumps of amyloid protein are usually associated with Alzheimer’s disease, but reports from the conference showed that they are also present in the brains of people with dementia with Lewy bodies. This means we should be considering whether some people affected by dementia with Lewy bodies could benefit from the anti-amyloid treatments that are currently in development for people with Alzheimer’s disease.
Stopping the spread between brain cells
Several sessions at the conference focused on disease processes that are shared by more than one condition. A topic that I find especially intriguing is the spreading of damaged, toxic proteins between brain cells. This has been observed in Parkinson’s, dementia with Lewy bodies and Alzheimer’s disease. In Parkinson’s and dementia with Lewy bodies, a protein called alpha-synuclein is the culprit. In Alzheimer’s it is the tau protein that passes between interconnected brain regions, seemingly bringing the damage of brain cells as it spreads.
Tau spreading was first discovered in 2009 and since then it has been observed in cells in a dish, in animal models and in the brains of people with dementia. Importantly, in people with Alzheimer’s disease, the movement of toxic tau from an area of the brain called the entorhinal cortex to the rest of the brain correlates with the development and progression of dementia symptoms. This discovery opens up a whole new avenue for developing treatments.
One approach being explored is to use antibodies that bind to the tau. This treatment aims to ‘mop up’ tau after it has been released by damaged brain cells and before it can be taken up by neighbouring cells. Researchers hope this will reduce how much tau spreads across the brain and therefore might slow down cognitive decline. The first vaccine against tau has been tested for safety by the biotech company AXON Neuroscience and is currently being tested for beneficial effects in people with mild to moderate Alzheimer’s disease in a small, early stage trial.
Abnormal tau protein is also a hallmark of frontotemporal dementia, a condition that currently has no treatments. AXON Neuroscience also discussed how their tau vaccine can trigger the production of useful antibodies in people with frontotemporal dementia. They will begin a clinical trial of the vaccine in people with a specific kind of frontotemporal dementia called primary progressive aphasia later in 2017.
Collaboration is the key to progress
This was my first time at the ADPD Congress and I was curious to learn how the two different research fields would come together. There was clearly an expanse of common ground between them in terms of the research techniques being developed and the molecular pathways and cellular mechanisms being explored. It was encouraging to see researchers working on one condition learning from the successes and failures of those working in a related disease area. This is another example of how being United Against Dementia is so important for progress to be made in finding much needed treatments for a number of different conditions.
Friday 7 April 2017
Finding the common ground between Alzheimer’s and Parkinson’s at the ADPD conference
Dr Clare Walton from our research team has just returned from the Alzheimer’s and Parkinson’s disease Congress (also known as ADPD), which was held in Vienna from 29 March to 2 April 2017. Here she reflects on the latest research she saw there.
Timeline of landmark discoveries in Alzheimer’s disease at ADPD. Photo credit: @thegblab on Twitter
The Alzheimer’s and Parkinson’s Disease (ADPD) Congress happens every two years. It brings together over 3,000 researchers from the field of neurodegeneration. This includes specialists in Alzheimer’s and Parkinson’s diseases but also on Parkinson’s disease dementia, Lewy body dementia, frontotemporal dementia and some other rarer conditions. From a clinical perspective, bringing these research fields together to share their latest findings makes a lot of sense. Although we define each of these forms of dementia as different conditions, we are increasingly learning that there is overlap between them.
Learning from each other
Several speakers, including Dr Lauren Walker from the University of Newcastle, reported that it is common to find that people have the biological hallmarks of more than one type of dementia in their brain. These hallmarks can be seen in a person’s brain tissue after they have died and, more recently, also in living people using innovative new brain imaging techniques.
Perhaps unsurprisingly, people who show signs of more than one type of dementia experience faster declines in cognitive function. These findings have important implications for the treatment of people with dementia. For example toxic clumps of amyloid protein are usually associated with Alzheimer’s disease, but reports from the conference showed that they are also present in the brains of people with dementia with Lewy bodies. This means we should be considering whether some people affected by dementia with Lewy bodies could benefit from the anti-amyloid treatments that are currently in development for people with Alzheimer’s disease.
Stopping the spread between brain cells
Several sessions at the conference focused on disease processes that are shared by more than one condition. A topic that I find especially intriguing is the spreading of damaged, toxic proteins between brain cells. This has been observed in Parkinson’s, dementia with Lewy bodies and Alzheimer’s disease. In Parkinson’s and dementia with Lewy bodies, a protein called alpha-synuclein is the culprit. In Alzheimer’s it is the tau protein that passes between interconnected brain regions, seemingly bringing the damage of brain cells as it spreads.
Tau spreading was first discovered in 2009 and since then it has been observed in cells in a dish, in animal models and in the brains of people with dementia. Importantly, in people with Alzheimer’s disease, the movement of toxic tau from an area of the brain called the entorhinal cortex to the rest of the brain correlates with the development and progression of dementia symptoms. This discovery opens up a whole new avenue for developing treatments.
One approach being explored is to use antibodies that bind to the tau. This treatment aims to ‘mop up’ tau after it has been released by damaged brain cells and before it can be taken up by neighbouring cells. Researchers hope this will reduce how much tau spreads across the brain and therefore might slow down cognitive decline. The first vaccine against tau has been tested for safety by the biotech company AXON Neuroscience and is currently being tested for beneficial effects in people with mild to moderate Alzheimer’s disease in a small, early stage trial.
Abnormal tau protein is also a hallmark of frontotemporal dementia, a condition that currently has no treatments. AXON Neuroscience also discussed how their tau vaccine can trigger the production of useful antibodies in people with frontotemporal dementia. They will begin a clinical trial of the vaccine in people with a specific kind of frontotemporal dementia called primary progressive aphasia later in 2017.
Collaboration is the key to progress
This was my first time at the ADPD Congress and I was curious to learn how the two different research fields would come together. There was clearly an expanse of common ground between them in terms of the research techniques being developed and the molecular pathways and cellular mechanisms being explored. It was encouraging to see researchers working on one condition learning from the successes and failures of those working in a related disease area. This is another example of how being United Against Dementia is so important for progress to be made in finding much needed treatments for a number of different conditions.
I am no longer able to hold your hand my beloved but I cherish the remembrance of your hand in mine...and the wonderful person that touched so many lives with joy. : )