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LC3-associated molecular pathways

LC3-associated endocytosis (LANDO) is a pathway we identified with Dr. Douglas Green at St. Jude Children's Research Hospital, that utilizes components of the autophagy machinery to conjugate LC3 to endosomes. Drs. Green and Heckmann found that LANDO is critical for the recycling of certain receptors on microglia including those that recognize beta-amyloid, a contributing factor to Alzheimer's Disease. Moreover, they identified a role for LANDO in mitigating neuroinflammation and preventing neurodegeneration.

While it is clear LANDO is protective against neuroinflammation and facilitates receptor recycling in microglia, the mechanism by which LANDO prevents inflammatory activation and polarization of microglia remains elusive. This project is designed to investigate the underlying relationships of LANDO and canonical pathways of inflammatory immune regulation in an effort to not only identify the linking mechanism, but to exploit those findings  as an avenue for targeted therapeutic development.

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Alzheimer's Disease & neurodegeneration

At the very heart of the Heckmann Lab is Alzheimer's Disease. This devestating neurodegenerative disease lacks any meaningful therapy to date. Characterized by the deposition of protein aggregates called amyloid plaques and symptomatic profiles of memory loss and behavioral changes, AD is as challanging on caregivers as it is on patients.

With the discovery of LANDO and the work from other groups demonstrating robust changes in microglia and neuroinflammation in both murine models and AD patients, there is new hope in potentially targeting inflammation and the regulatory pathways which govern it in AD and other neurodegenerative conditions. We are building upon the indentification of LANDO and its protective role in AD pathology by explore new regulators of both LANDO and inflammatory mechanisms in microglia as a whole. We are currently partnering with biotech and pharmaceutical companies to use our findings to help develop new therpaeutic modalities for AD and beyond. 

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Immune regulation in ischemic stroke

Microglia function and neuroinflammation are known aspects of vacular ischemia including acute ischemic stroke. The role of the autophagy machienry and LC3-associated molecular pathways in stroke remain poorly understood.

We are taking a multifaceted approach to better understand the underlying biology of stroke and reperfusion injury and the role microglia play in this process. Furthermore, we are attempting to design novel avenues for therapeutic intervention to both stroke as well as applications to prevent post-stroke or post-reperfusion injury.

Versatility in Application

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Neuroimmune mapping & profiling

To better understand how neuroinflammation is impacting diseases of the central nervous system including Alzheimer's Disease and stroke, we are developing novel methods of cytokine tracing using MRI analysis paired with transcranial multiphoton imaging to "map" the neuroimmune architecture during development and pathology.

We are combining these new cutting edge imaging modalities with spatial transcriptomics in a variety of pathological settings starting with Alzheimer's Disease.

By profiling the neuroimmune architecture under varying conditions, we now have the capacity to compare and contrast brain-region specific microglial responses and the impact changes in microglial biology have on other cells including neurons. Cumulatively, we hope these findings will lead to the advancement of targeted interventions that exploit specific cell signatures for therapuetic gain.

We Integrate With Your Ecosystem

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Sleep biology and immunity

Circadian rhythms control and influence a host of biological processes and are highly governed by sleep. A long standing question has focused on why we need to sleep in the context of immune function. 

Sleep loss and the inability to properly rest is a major symptom of Myalgic Encephalomyelitis/chronic fatigue syndrome. ME/CFS is a unique set of symptoms that typically arises following a bacterial or more commonly viral infection with idiopathic etiology. ME/CFS has garnered significant attention with the COVID-19 pandemic and long-haul COVID patients. We are explore the role of sleep and neuroimmune function in ME/CFS in hopes of finding new targets for this mysterious and often neglected condition.

 

Thus far, we have strong preliminary evidence that this form of sleep disruption effects immune pathways in microglia as well as genes that regulate these pathways.