Neurodegenerative disease like Alzheimer's and Parkinson’s are progressive disease that causes great suffering for the victims and relatives, in addition it cause large economic costs for society.
The prevalence of these diseases increases almost exponentially with age after 60 years and with increasing life-span the number of affected people is expected to rise rapidly.
Bild 1
In Alzheimer’s disease this is seen as initial memory problems, followed by other cognitive functions until the patient eventually cannot handle activities of daily life and requires full care giving.
In the brain this is evident as successive spread of the pathology from certain brain areas, such as the hippocampus, to others. It has long been known that this recruitment of new areas follows anatomical pathways but the messenger of the propagation has remained elusive. The neuropathological characteristic is plaques and tangles, composed mainly of β-amyloid (Aβ) and abnormally phosphorylated tau. (Picture 1)
However, the pathological processes start inside the neurons long before plaques and tangles are seen. Similar propagation is seen in Parkinson’s disease where aggregation of alfa-synuclein into Lewy bodies are characteristic for the disease.
My lab is working to identify and understand these early processes and why they propagate through the brain.
We have showed that intracellular, toxic forms of the protein beta-amyloid can propagate from neuron-to-neuron via the connections between the long processes of the neurons, the axons and the dendrites. (Picture 2)
A few days after this spread we could show that the receiving cells get sick. Thus, intracellular beta-amyloid oligomers seems to be the elusive messenger propagating Alzheimer’s disease from one neuron to another, one brain area to another.
Our current studies are focusing on understanding the mechanisms of neuron-to-neuron spread of aggregates of different misfolded proteins, such as beta-amyloid and alpha-synuclein oligomers. Furthermore, we want to understand how the transferred protein aggregates cause adverse effects in the receiving cells.
This includes understanding intra-cellular transport machinery and degradative systems. To understand the intra- and extracellular events important for the spread and toxicity of misfolded proteins we are actively working to develop our unique toolbox of relevant cellular models. We also want to find ways to stop this propagation of neurodegenerative diseases.
To understand the mechanisms of the continuous progression of neurodegenerative diseases, find out if these are similar for different neurodegenerative proteins and using this knowledge to stop the progrssion of disease. Altogether, this is an innovative project with the potential to yield new and important knowledge on neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
Bild 1
In Alzheimer’s disease this is seen as initial memory problems, followed by other cognitive functions until the patient eventually cannot handle activities of daily life and requires full care giving.
Bild 2
In the brain this is evident as successive spread of the pathology from certain brain areas, such as the hippocampus, to others. It has long been known that this recruitment of new areas follows anatomical pathways but the messenger of the propagation has remained elusive. The neuropathological characteristic is plaques and tangles, composed mainly of β-amyloid (Aβ) and abnormally phosphorylated tau. (Picture 1)
However, the pathological processes start inside the neurons long before plaques and tangles are seen. Similar propagation is seen in Parkinson’s disease where aggregation of alfa-synuclein into Lewy bodies are characteristic for the disease.
My lab is working to identify and understand these early processes and why they propagate through the brain.
We have showed that intracellular, toxic forms of the protein beta-amyloid can propagate from neuron-to-neuron via the connections between the long processes of the neurons, the axons and the dendrites. (Picture 2)
A few days after this spread we could show that the receiving cells get sick. Thus, intracellular beta-amyloid oligomers seems to be the elusive messenger propagating Alzheimer’s disease from one neuron to another, one brain area to another.
Our current studies are focusing on understanding the mechanisms of neuron-to-neuron spread of aggregates of different misfolded proteins, such as beta-amyloid and alpha-synuclein oligomers. Furthermore, we want to understand how the transferred protein aggregates cause adverse effects in the receiving cells.
This includes understanding intra-cellular transport machinery and degradative systems. To understand the intra- and extracellular events important for the spread and toxicity of misfolded proteins we are actively working to develop our unique toolbox of relevant cellular models. We also want to find ways to stop this propagation of neurodegenerative diseases.
To understand the mechanisms of the continuous progression of neurodegenerative diseases, find out if these are similar for different neurodegenerative proteins and using this knowledge to stop the progrssion of disease. Altogether, this is an innovative project with the potential to yield new and important knowledge on neurodegenerative diseases such as Alzheimer’s and Parkinson’s.
Foto: Thor Balkhed
