Jeffrey Nicholas Savas
Northwestern University, IL·Neuroscience
Alzheimer's disease (AD) is an incurable brain disorder affecting more than five million people in the United States. Its signature marks are amyloid plaques, which are clumps of a small protein fragment called amyloid beta (Aβ) that build up between brain cells.
- Fields
Neuroscience
Biochemistry
- Topics
Alzheimer's disease
amyloid beta
Aβ42
- Grants
- 1 known grant, through May 2027
What they work on
- Build a dynamic map of how amyloid beta (Aβ) plaques form and change in the brains of aging Alzheimer's model mice, tracking distinct plaque classes and Aβ forms such as Aβ42 and Aβ38.
- Determine how Trem2, a gene linked to Alzheimer's risk, influences the behavior of Aβ, lipids and proteins at amyloid plaques in mouse model brains.
- Combine the multi-omic plaque maps with measures of altered communication between nerve cells and of nerve cell damage, to link plaque development to synapse dysfunction.
- Turn the plaque findings into 3D brain maps that other neuroscience researchers can use.
More about the research
Drugs that clear plaques have recently been approved, yet it is still unclear how plaques form over time, how varied they are, and how they harm or protect the nerve circuits around them. This project aims to map how plaques develop during the early stages of disease.
Why it matters
Recently approved Alzheimer's drugs target amyloid plaques, but how plaques form and cause damage is still poorly understood. Knowing which plaque types form early and how they disrupt communication between nerve cells could show when and where treatments act best. For the millions of people with Alzheimer's disease, this could guide better plaque-targeting therapies. The project's 3D plaque maps will also be shared with the neuroscience community as a resource.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Riqiang Yan
University of Connecticut, CT·Neuroscience
Identify potent short peptides from the CX3CL1 C-terminal domain (CX3CL1-ICD), a neuron-protecting protein region, that reduce Alzheimer's pathology and cell death in neurons and AD mouse models.
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.
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.
The school
Northwestern University: 71 labs on PI Pages, $1.3B a year on research, 536 research doctorates a year.
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