About

Tyler Ulland holds an MS and PhD and is an Associate Professor of Pathology and Laboratory Medicine at the University of Wisconsin–Madison. He is also recognized as a Vilas Early-Career Investigator. His role involves leading research in the field of pathology and laboratory medicine, with a focus on innate immunology of neurodegeneration. As a faculty member, he contributes to advancing understanding in this area, although specific details of his research focus and key contributions are not provided in the page text.

Research topics

• Biology
• Medicine
• Neuroscience
• Pathology
• Immunology
• Endocrinology
• Genetics
• Internal medicine

Selected publications

• β-Hydroxybutyrate inhibits inflammasome activation to attenuate Alzheimer’s disease pathology

  Journal of Neuroinflammation · 2020 · 241 citations

  Senior authorCorresponding
  • Medicine
  • Neuroscience
  • Internal medicine

  Alzheimer's disease (AD) is a progressive, late-onset dementia with no effective treatment available. Recent studies suggest that AD pathology is driven by age-related changes in metabolism. Alterations in metabolism, such as placing patients on a ketogenic diet, can alter cognition by an unknown mechanism. One of the ketone bodies produced as a result of ketogenesis, β-hydroxybutyrate (BHB), is known to inhibit NLRP3 inflammasome activation. Therefore, we tested if BHB inhibition of the NLRP3 inflammasome reduces overall AD pathology in the 5XFAD mouse model of AD. Here, we find BHB levels are lower in red blood cells and brain parenchyma of AD patients when compared with non-AD controls. Furthermore, exogenous BHB administration reduced plaque formation, microgliosis, apoptosis-associated speck-like protein containing a caspase recruitment domain (Asc) speck formation, and caspase-1 activation in the 5XFAD mouse model of AD. Taken together, our findings demonstrate that BHB reduces AD pathology by inhibiting NLRP3 inflammasome activation. Additionally, our data suggest dietary or pharmacological approaches to increase BHB levels as promising therapeutic strategies for AD.

  DOI

• The Role of Microglia and the Nlrp3 Inflammasome in Alzheimer's Disease

  Frontiers in Neurology · 2020 · 233 citations

  Senior authorCorresponding
  • Neuroscience
  • Medicine
  • Immunology

  Alzheimer's disease (AD) is the most prevalent form of late-onset dementia. AD affects the health of millions of people in the United States and worldwide. Currently, there are no approved therapies that can halt or reverse the clinical progression of AD. Traditionally, AD is characterized first by the appearance of amyloid-β (Aβ) plaques followed by the formation of intraneuronal neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau (p-tau). These lesions are linked to synapse loss and eventual cognitive impairment. Additionally, microgliosis is consistently found in regions of the brain with AD pathology. The role of microglia in AD onset and progression remains unclear. Several recent reports indicate that the assembly of the multi-protein complex known as the NOD, LRR, and pyrin-domain containing 3 (Nlrp3) inflammasome by microglia results in apoptosis spec-like protein containing a CARD (Asc) spec formation, which then nucleates new Aβ plaques, thus amplifying Aβ-associated pathology. NFTs can also activate the Nlrp3 inflammasome leading to enhanced tau-associated pathology. Here, we will review the role of microglia and the activation of the inflammasome in the innate immune response to AD.

  DOI

• Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer’s disease

  Nature Medicine · 2020 · 1175 citations

  • Neuroscience
  • Biology
  • Medicine
  DOI

Recent grants

• Fetal reprogramming by gestational intermittent hypoxia impairs respiratory neuromotor control in adult offspring

  NIH · $3.0M · 2019–2024

• Sugar Utilization by Microglia in Alzheimer's Disease

  NIH · $426k · 2020–2022

• Gut barrier function in Alzheimer’s disease

  NIH · $3.9M · 2021–2026

Frequent coauthors

• Henrik Zetterberg

  UK Dementia Research Institute

  24 shared

• Sanjay Asthana

  Geriatric Research Education and Clinical Center

  23 shared

• Marco Colonna

  Hope Center for Neurological Disorders

  23 shared

• Fayyaz S. Sutterwala

  Cedars-Sinai Medical Center

  20 shared

• Sterling C. Johnson

  Temple University

  19 shared

• Kaj Blennow

  University of Gothenburg

  17 shared

• Barbara B. Bendlin

  University of Wisconsin–Madison

  17 shared

• Federico E. Rey

  University of Wisconsin–Madison

  16 shared

Labs

• The Ulland LabPI

Education

• PhD, Molecular and Cellular Biology

  University of Iowa Graduate College

  2014

• MS, Immunology

  University of Iowa Graduate College

  2010

• BA, Biochemistry and Molecular Biology

  Cornell College

  2006

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