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Young neurobiologists awarded grants for Alzheimer´s and Parkinson´s research

A dark silhouette of a head against a blue background. Illustration.
Image: Ben Sweet

Two young experimental researchers have been awarded grants from the Anna-Lisa Rosenberg Foundation, the Department of Experimental Medical Science´s own grant for research in the neurobiological field with a clinical collaboration.

Congratulations Alessandro Fiorenzano on the Anna-Lisa Rosengren Foundation grant, 65 000 SEK, how does it feel?
– I am grateful for this fantastic opportunity!

What does the grant mean for you and your research? I´m a Senior Postdoc, and this grant will help me to develop my own independent line of research in the stem cell and regenerative medicine field by combining my previous scientific experience with new skills acquired during my postdoctoral training at Lund University.

How will you use the grant?
– This grant will feed my research for a generation of mini-brains in a dish to study  dopamine neuron function and disease.

Tell us about your research.
– 
My current focus is on deciphering the molecular signature of human dopamine neurons for enhanced patient-specific cell therapy in Parkinson´s disease.

 Why is this area interesting?
– The ability to recreate human dopamine neurons from pluripotent stem cells is a great opportunity to study maturation and function of human dopamine neurons. This also provides access to a renewable source of cells potentially suitable for human brain repair. 

Tell us about this particular project you have received funding for.
– In this project I will use cutting edge sequencing technology to investigate molecular identity of human dopamine neurons derived from human brain organoids and  xenografts in Parkinson's Disease rat model. This approach could break down the intricate regulatory systems controlling dopamine neuron differentiation into individual layers, providing new and fundamental knowledge at an unprecedented level of detail and sophistication of as yet unknown transcription factors and molecular cues specifically driving human  dopamine neuron diversity.

What benefit can new knowledge in this field contribute?
– This project will provide mechanistic insights into dopamine neuron subtypes specification to refine differentiation protocols for therapeutic use.

Congratulations Isak Martinsson on the Anna-Lisa Rosengren Foundation grant, 65 000 SEK! A sports question, how does it feel? 
– It feels great and I’m grateful for the opportunity to test out my hypotheses.
What does the grant mean for you and your research? 
– This grant means that I can order equipment and reagents necessary to test an idea I’ve been obsessing with for some years now. It also means that other researchers see the potential interest in the subjects I’m pursuing.
How will you use the grant? 
– I will use it to purchase micro-electrode array culture plates which allow continuous electrical recordings from cultured neurons and reagents.
Tell us about your research.
– For the brain to function properly multiple feedback mechanisms need to function in concert. The brain is somehow able to both maintain flexibility (plasticity) and stability. When we learn new things, the neurons in our brains change, specifically at synapses, the places where communication between neurons occurs. These changes strengthen or weaken specific “pathways” and thereby influence the probability of certain networks to activate. These modifications of synaptic strengths are termed Hebbian Synaptic plasticity. However, if these mechanisms of plasticity are allowed to operate freely, they can lead to destabilization of neuronal networks. Thus, to preserve the stability of neuronal networks there is a balancing mechanism called homeostatic synaptic plasticity. This negative feedback mechanisms regulates the activity at the neuron and network level to maintain stability in neuronal networks. It is easiest to imagine it as a sort of tuning mechanism to make sure that signals are clear.
Recently the proteins that have been suggested to be involved in Alzheimer’s disease were implicated in regulating this “homeostatic synaptic plasticity”. I investigated how cultured neurons from a mouse model of Alzheimer’s disease were unable to induce homeostatic synaptic plasticity in response to chronic hyperactivity.
Why is this area interesting?
– 
Alzheimer’s disease and other neurodegenerative disorders are currently incurable diseases which cause tremendous suffering for the afflicted and high costs for society, since they lead to a state were patients require constant care. Homeostatic synaptic plasticity mechanisms are also very interesting since the field continuously advances and more and more research connects not only neuronal mechanisms but also implicate astrocytes and microglia as potential regulators.  
Tell us about the particular project you have received funding for.
– The project I was awarded for is named Amyloid precursor protein and its role as a rheostat in neuronal activity. Both epileptic seizures and traumatic brain injury causes lesions that are similar to those seen in Alzheimer’s disease. Since both epilepsy and traumatic brain injury lead to massive global alteration in neuronal activity these changes need to be compensated and therefore likely include homeostatic plasticity. Here I proposed to study how chronic changes in activity levels affect the Amyloid precursor protein, which is a protein that has been genetically linked to Alzheimer’s disease, but also how the lack of Amyloid precursor protein in genetically modified neurons respond to chronic changes in activity. 
What benefit can new knowledge in this field contribute? 
– Since both traumatic brain injury and epileptic seizures accelerate Alzheimer’s disease pathology and progression understanding how homeostatic mechanisms normalize the brain activity after these insults could provide new insights to the role of the Alzheimer’s related Amyloid precursor protein and its cleavage products have in regulating neuronal activity. If it turns out that homeostatic plasticity mechanisms are severely impaired in Alzheimer’s disease this could potentially be a target for therapies.

The Anna-Lisa Rosenberg Foundation

According to the will of Anna-Lisa Rosenberg, part of her assets will give a yearly income to the “department of neurological science, Sölvegatan 19 in Lund”. Grants are to be awarded once a year and for one year at the time. Applicants affiliated to The Department of Experimental Medical Science, holding a PhD and being in the early stage of their career are prioritised. Projects should preferably be carried out within the neurobiological field and contain a clinical collaboration.

Outdoors profile photo of Isak Martinsson.
Photo: Agata Garpenlind

Isak Martinsson

Postdoc in Experimental dementia research unit and experimental neuroinflammation laboratory.

isak [dot] martinsson [at] med [dot] lu [dot] se

Link to Isak Martinsson's profile in the LU Research Portal

Profile photo of Alessandro Fiorenzano. Photo.

Alessandro Fiorenzano

Postdoc in Developmental and Regenerative Neurobiology

alessandro [dot] fiorenzano [at] med [dot] lu [dot] se

Link to Alessandro Fiorenzano's profile in the LU Research Portal