Mariana Potcoava
University of Illinois Chicago, IL·Neuroscience·Early-career
Alzheimer's disease (AD) is the most common cause of dementia and has no effective treatment. By the time it is diagnosed, many neurons have already died.
- Fields
Neuroscience
Biophysics
Physics
- Topics
Alzheimer's disease
dementia
neurodegeneration
- Grants
- 1 known grant, through Apr 2029
What they work on
- Test whether presynaptic Ca2+ signaling and homeostasis drive loss of synaptic transmission at hippocampal excitatory synapses in humanized APOE4 mouse models of Alzheimer's disease.
- Image fast events of synaptic transmission, including neurotransmitter release, at high speed and with minimal light damage using a lab-built lattice light-sheet microscope.
- Apply a lattice light-sheet imaging method based on incoherent holography to visualize synaptic function in intact neural tissue without moving the detection objective.
- Examine how amyloid β and APOE genotype contribute to presynaptic dysfunction in mouse models of neurodegeneration.
More about the research
That neuron loss follows an earlier loss of synapses, the junctions where neurons pass signals, so synapse failure is an early part of the disease. This project uses fast, gentle microscopy to watch how synapses fail in mouse models of AD, focusing on the hippocampus, a memory center affected early in patients.
Why it matters
Synapse failure comes before neuron loss in Alzheimer's disease, and APOE genotype and amyloid β are key drivers of the disease. Watching how presynaptic signaling breaks down in mouse models could clarify early mechanisms of cognitive decline. The gentle, high-speed imaging methods developed here could also aid other studies of the aging and neurodegenerating brain.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Martin Hruska
West Virginia University, WV·Neuroscience
Test how acute amyloid-beta affects PSD-95 stability in spines with different numbers of nanomodules. Use live-cell STED super-resolution imaging, with CRISPR tags on the neurons' own PSD-95 and AMPA receptors.
Giuseppina Tesco
Tufts University, MA·Neuroscience
Test whether the ABCA7 p.Ala1527Gly variant lowers ABCA7 protein levels and causes loss of function in iPSC-derived human excitatory neurons, measuring Aβ42/40 ratios, a readout of harmful amyloid-β.
Wenzhang Wang
Case Western Reserve University, OH·Neuroscience
Determine whether and how abnormally increased contacts between mitochondria and the endolysosomal system cause mitochondrial defects in Alzheimer's disease neurons, using in vivo and in vitro disease models.
The school
University of Illinois Chicago: 42 labs on PI Pages, $532M a year on research, 359 research doctorates a year.
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