Allison L Kraus
Case Western Reserve University, OH·Neuroscience
Tau is a protein that normally helps keep nerve cells structurally stable, but in Alzheimer's disease and several related dementias it misfolds and spreads through the brain. Misfolded tau can act as a "seed": it can force normal tau to misfold too, much like prions do.
- Fields
Neuroscience
Medicine & Clinical Research
Biochemistry
- Topics
tau
Alzheimer's disease
frontotemporal lobar degeneration
- Grants
- 2 known grants, through Nov 2030
What they work on
- Define the age of onset, amount, brain location and chemical variety of tau seeds in diseased, normal, young and older human brains, using RT-QuIC seed amplification assays specific to 3R, 4R and 3R/4R tau.
- Test how post-translational modifications, chemical tags added to tau after it is made, and co-occurring α-synuclein clumps change tau seeding, using seed detection, biochemical assays, immunomapping and structural profiling.
- Map cell states around tau seeds across disease stages with proteomics, single-nucleus RNA sequencing and spatial transcriptomics, which measure gene activity cell by cell and in place in brain tissue.
- Determine how myeloid and glial cells, the brain's immune and support cells, spread or clear tau seeds, including how inflammatory reactive oxygen species alter seeding ability.
- Establish tau-seeding activity in skin, measured by RT-QuIC and PMCA amplification assays, as a biomarker for diagnosing Alzheimer's disease in autopsy samples and in living patients, and for predicting their clinical outcomes.
- Test whether skin tau-seeding distinguishes Alzheimer's from other tauopathies and from Lewy body dementia, and whether it is detectable before symptoms in animal models of tau disease.
More about the research
Two questions run through these projects. When and where do these seeds first appear, and what makes them grow or shrink? And can seeds found outside the brain, in skin, serve as a practical test for these diseases?
Why it matters
Alzheimer's disease and related dementias can only be confirmed by examining the brain after death. A skin test for misfolded tau could give patients an earlier and more specific diagnosis, help tell Alzheimer's apart from Lewy body dementia, and track treatment response in clinical trials. Mapping where and when tau seeds first form in the brain, and which immune and cellular conditions favor them, may reveal targets for blocking tau spread at its earliest and most important stages.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Mohammad Shahnawaz
University of Texas Health Science Center at Houston, TX·Neuroscience
Detect and amplify small amounts of alpha-synuclein strains from body fluids and brain tissue of patients with Parkinson's disease, multiple system atrophy and dementia with Lewy bodies, using the seeding-based PMCA (RT-QuIC) assay.
David John Irwin
University of Pennsylvania, PA·Neuroscience
Test whether FTLD-Tau and FTLD-TDP show distinct layer-specific and regional patterns of iron-rich gliosis (activated support cells) in postmortem brain, using multiplexed immunofluorescence and 7T MRI-guided digital histology of the Penn FTLD brain bank.
Daniel Lee
University of Kentucky, KY·Neuroscience
Test how the arginine sensor CASTOR1, a brake on the growth regulator mTORC1, improves lysosome function, repair and clearance of protein clumps when cell models are stressed by tau or lysosome-damaging agents.
The school
Case Western Reserve University: 34 labs on PI Pages, $643M a year on research, 213 research doctorates a year.
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