Treating Memory Loss in Alzheimer's Disease by Strengthening Synapses

Camin Dean, PhD
German Center for Neurodegenerative Disease (Goettingen, Germany)
Year Awarded:
2019
Grant Duration:
July 1, 2019 to June 30, 2022
Disease:
Alzheimer's Disease
Award Amount:
$300,000
Grant Reference ID:
A2019586S
Award Type:
Standard
Award Region:
International

Treating Memory Loss in Alzheimer's Disease by Strengthening Synapses

Summary

People with Alzheimer's disease lose the ability to remember things, especially things they recently learned. We recently discovered that mice missing a specific molecule called Synaptotagmin3, have better memory than normal mice. We now want to test if removing this molecule from mice with Alzheimer's disease will improve their memory. If this works, it could be a way to treat humans with Alzheimer's disease to improve their memory.

Details

People with Alzheimer's disease lose the ability to remember things, especially things they recently learned. We recently discovered that mice missing a specific molecule called Synaptotagmin3, have better memory than normal mice. We now want to test if removing this molecule from mice with Alzheimer's disease will improve their memory. If this works, it could be a way to treat humans with Alzheimer's disease to improve their memory.

About the Researcher

Camin Dean received her Ph.D. from the University of California, Berkeley where she performed pioneering work on molecules that regulate the assembly of synapses. In her postdoctoral research at the University of Wisconsin, Madison, she extended her work to synapse function, and discovered molecular mechanisms by which brain-derived neurotrophic factor (BDNF) is trafficked and released to affect synapse strength in circuits related to memory. Since 2010, she is an independent group leader at the European Neuroscience Institute in Göttingen, Germany, where she continues to study molecules important for synapse formation and function and that underly remembering and forgetting.

Personal Story

Until recently, my scientific interests had always been driven by a basic curiosity of how exactly connections between neurons can change - to encode new memories, keep the important ones, and erase those that are no longer needed.  But when we found that removal of a specific molecule from synapses in mice causes them to no longer forget, I realized we could manipulate this molecule to improve memory in cases of "too much" forgetting, in Alzheimer's disease.  I am grateful to the Brightfocus Foundation for allowing us to test this idea and to now directly contribute to research aimed at treating Alzheimer's disease.

Don't miss out.
Receive research updates, inspiring stories, and expert advice
Please enter your first name.
Please enter your last name.
Keep me informed about: *
Please select at least one.
You must select at least one disease category.