Research Interests:
Blood-brain Barrier Physiology, Traumatic Brain Injury and Stroke, Neuroinflammation and Neurodegeneration, Alzheimer's Disease and Related Dementias, Neuropharmacology and Brain-drug Delivery, Glycobiology and Glycomics
Dr. Aric Logsdon - Faculty Page
Aric F. Logsdon, PhD
Assistant Professor
Texas Tech University Health Sciences Center
Dr. Aric Logsdon is an experienced biomedical researcher with a strong neuroscience background and expertise in preclinical drug discovery for human neurological disease. Aric earned his PhD in Pharmaceutical Sciences from West Virginia University in 2016 and completed Postdoctoral training at the University of Washington under the mentorship of Dr. William A. Banks. Dr. Logsdon recently held a faculty appointment with the University of Washington School of Medicine and also served as a Health Science Specialist for the US Department of Veterans Affairs.
Dr. Logsdon has published over 50 peer-reviewed publications in high-impact scientific journals, including: Nature Neuroscience, Nature Metabolism, Nature Aging and Alzheimer’s & Dementia. Aric is an acknowledged expert in neuroscience research and has been invited to chair sessions and present lectures of his work at multiple national and international scientific conferences. Dr. Logsdon is also the recipient of several honors and awards from research societies, including: Psychoneuroimmunology Research Society, the International Society for Cerebral Blood Flow and Metabolism, and the National Neurotrauma Society.
Dr. Logsdon is interested in elucidating the functional role(s) of brain glycans in preclinical models of neuroinflammation. Dr. Logsdon employs innovative biochemical techniques to measure brain glycan composition, blood-brain barrier function and the pathogenesis of neurodegeneration. Dr. Logsdon seeks to determine the causal relationship(s) between cerebrovascular dysfunction, brain glycan changes, and the development of Alzheimer’s disease clinicopathology. Results from this research may lead to novel drug discovery efforts for treating human neurological diseases.
Current Projects:
Elucidating a novel mechanism of intracellular brain glycan accumulation in traumatic brain injury. Traumatic brain injury (TBI) is a chronic health condition affecting over 70,000 individuals per year. Multiple lines of evidence suggest TBI as a notable risk factor for the development of cognitive impairment through converging biological mechanisms that are poorly understood. Therefore, a dire need for innovative approaches to better understand the biological mechanisms induced by TBI is required for clinical success to reduce the development of cognitive impairment. Ubiquitin Carboxy-terminal Hydrolase L1 (UCHL1) is an established biomarker for TBI and regulates brain protein homeostasis. TBI-induced inflammatory factors (e.g., prostaglandins and nitric oxide) interact with UCHL1 and diminish its ability to remove aberrant proteins from brain cells. We recently discovered a progressive accumulation of brain glycans in UCHL1-positive cells of mice exposed to TBI. Understanding the mechanism(s) of brain glycan accumulation will lead to novel therapeutic strategies to slow the course of TBI-related cognitive impairment. This project focuses on the intracellular processing of brain glycans under neuroinflammatory conditions. Our lab seeks to determine whether UCHL1 plays a vital role in regulating brain glycan homeostasis. In collaboration with the University of Pittsburgh, we will obtain access to a neuroprotective mouse line which have a mutation (C152A knock-in) in the UCHL1 protein domain that has been shown to resist PG and NO interactions under neuroinflammatory conditions. We hypothesize that when C152A mice are exposed to TBI, we will discover a reduction in brain glycan accumulation. Our lab also seeks to explore whether drugs targeting the C152A domain of UCHL1 will improve TBI outcomes through mechanisms of brain glycan accumulation. If fully successful, results will suggest UCHL1 to play a major role in TBI-induced neurobehavioral dysfunction through mechanisms of brain glycan accumulation.
Exploring glycan-protein interactions at the blood-brain barrier in cerebral amyloid angiopathy. Alzheimer’s disease (AD) is a major health problem affecting approximately 5.8 million people in the US. The ‘vascular hypothesis’ of AD has regained momentum, and multiple lines of evidence have implicated vascular blood-brain barrier (BBB) dysfunctions in the onset of AD. Cerebral amyloid angiopathy (CAA) is the most common vascular comorbidity found in AD, and is biologically defined by the increased perivascular accumulation of amyloid beta (Aβ) that accompanies cognitive decline. Multiple lines of evidence have implicated chondroitin sulfate glycosaminoglycan (CS-GAG) sulfation as being associated with Aβ accumulation, as being altered in AD, and as possibly contributing to BBB dysfunction in CAA. This project will identify changes in CS-GAG sulfation in isolated brain microvessels (BMV) from individuals with CAA and from a rat model for human CAA. We will also determine whether GAG manipulations can affect perivascular Aβ binding and clearance in both a rat model for human CAA and in an in vitro model for the human BBB. Despite growing evidence for CS-GAG composition to play a role in the AD pathogenesis, technical issues of cross-reactivity in traditional immunohistochemical labeling of CS-GAG sulfation makes it nearly impossible to determine which CS-GAG isomers are associated with BBB dysfunction. A lack of quantitative methods to evaluate CS-GAG sulfation in human brain tissue has severely limited our ability to understand how CS-GAG composition contributes to the CAA pathogenesis. Addressing this limitation, we recently developed innovative liquid chromatography tandem mass spectrometry techniques capable of quantifying CS-GAG sulfation patterns from both rat and human brain tissue and recently discovered that human brain tissue from AD individuals exhibited a significant shift in CSGAG sulfation compared to non-AD controls. Here, we propose to identify, for the first time, CS-GAG sulfation patterns in BMVs from humans with CAA. Linking quantitative analyses of CS-GAG sulfation with cellular resolution is a critical step toward understanding how glycan-based mechanisms of BBB dysfunction may drive the CAA pathogenesis. CS-GAG sulfation patterns dictate glycan-protein interactions that can influence neurological function. There exists a strong correlation between CS-GAG sulfation and AD clinicopathology, where Aβ has been shown to accumulate within CS-GAG-rich extracellular spaces of the brain. We predict that a significant interaction between CS-GAGs and Aβ also exists at the BBB and may contribute to an impaired clearance of perivascular Aβ in CAA. Our central hypothesis is that CAA-related BBB dysfunction is influenced by changes in CS-GAG composition at the BBB. We will test our hypothesis by identifying the CS-GAG sulfation of BMVs from individuals with CAA, and by evaluating whether GAG manipulations can affect perivascular Aβ clearance in both a rat model for human CAA and in an in vitro model for the human BBB.
Current Funding:
- Start-up Funds from Texas Tech University Health Sciences Center Department of Pharmacology and Neuroscience and the Office of Research
- K22AG081264 NIH-NIA Logsdon (PI) 04/01/2025-03/31/2028 Pending
- R01NS143817 NIH-NINDS Logsdon (PI) 07/01/2025-06/30/2030 Pending
- R01AG096185 NIH-NIA Logsdon (PI) 07/01/2025-06/30/2030 Pending
Selected Publications:
- Logsdon AF, Foresi B, Hu SJ, Quah E, Meuret CJ, Le JP, Hendrickson AS et al., Perineuronal net deglycosylation associates with tauopathy-induced gliosis and neurodegeneration. J Neurochem. 2024. PMID: 38317026
- Logsdon AF, Francis KL, Richardson NE, Hu SJ, Faber CL, Phan BA, Nguyen V et al., Decoding perineuronal net matrix sulfation patterns in the Alzheimer’s disease brain. Alzheimer’s & Dementia. 2022. PMID: 34482642
- Alonge KM, Herbert MJ, Yagi M, Cook DG, Banks WA, Logsdon AF. Changes in Brain Matrix Glycan Sulfation Associate with Reactive Gliosis and Motor Coordination in Mice with Head Trauma. Front. Behav. Neurosci. 2021. PMID: 34776892
- Logsdon AF, Erickson MA, Chen X, Qui J, Lim Y, Stonestreet BS, Banks WA. Inter-alpha protein inhibitors attenuate inflammatory cytokines and blood-brain barrier disruption induced by lipopolysaccharide. JCBFM. 2020. PMCID: PMC7181088
- Alonge KM, Logsdon AF, Murphree TA, Banks WA, Keene CD, Edgar JS, Whittington D, Schwartz MW et al., Quantitative analysis of chondroitin sulfate disaccharides from human and rodent fixed brain tissue by electrospray ionization-tandem mass spectrometry. Glycobiology. 2019. PMCID: PMC6861844
Click here to see the complete List of Dr. Logsdon’s Published Work.