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A Reaction-Diffusion Model of Neurofibrillary Tangle Propagation through the Neocortex

Wednesday, February 5, 2020

2:00 PM-4:00 PM

BIOMED PhD Research Proposal

A Reaction-Diffusion Model of Neurofibrillary Tangle Propagation through the Neocortex as Represented by 18F Flortaucipir PET

Ian A. Kennedy, PhD Candidate
School of Biomedical Engineering, Science and Health Systems

Andres Kriete, PhD
Associate Dean for Academic Affairs
School of Biomedical Engineering, Science and Health Systems
Drexel University
Michael David Devous, Sr, PhD
VP, Imaging Development
Avid Radiopharmaceuticals
Alzheimer’s disease is a devastating neurodegenerative disease which affected approximately 5.7 million Americans in 2018 and is expected to grow exponentially by 2050 as the population ages. Those with AD required 18.4 billion hours of care, most of which is unpaid care from family members that costs, on average, almost $350,000 dollars per person.

Current hypotheses on the mechanism of AD incorporate the combined role of two proteins: beta amyloid plaques and neurofibrillary tangles (NFTs). Bet¬¬a amyloid is hypothesized to be the spark that ignites the hyperphosphorylation and destabilization of tau protein, leading to their agglomeration and eventual proliferation as NFTs. The phosphorylation of tau protein results in destabilization of neuronal microtubules, leading to the neuronal dysfunction, apoptosis and eventually regional atrophy of the brain. Cognitive decline increases as the disease worsens, generally thought to correlate with increasing spread of NFTs. Currently, AD is only able to be definitively diagnosed at autopsy, complicating the understanding the disease and validation of therapeutic clinical trials. The advent of amyloid- and tau-specific positron emission tomography (PET) tracers in conjunction with other imaging biomarkers has led to a hypothetical model of the progression of AD.  However, the mechanism of propagation of disease is still not well defined.

Quantitative and qualitative descriptions of the accumulation and advancement of NFTs throughout the neocortex from both in vitro pathologic staining and in vivo flortaucipir (FTP) PET imaging characterizes the propagation of NFTs by increasing local intensity and increasing spatial extent. The intensity-extent phenomenon is naturally encompassed through reaction-diffusion equations (RDEs) wherein the molecular mechanisms leading to tau accumulation in neurons represent the reaction and the expansion of tau with increasing disease stage along white matter trajectories is considered as a diffusion process. Application of RDE modeling may provide insight into the accumulation and propagation of NFTs as represented by FTP PET throughout the neocortex as well as the development of novel, tailored endpoints for anti-tau therapeutic trials.

Contact Information

Ken Barbee

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