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1. Infectious Diseases

Author

Li, Herman, Terrando, Niccolò, Gelbard, Harris A., Verkhratsky, Alexej, Series Editor, Tremblay, Marie-Ève, editor, and Verkhratsky, Alexei, editor

Published
2024
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3. Impact of COVID‐19 on the Onset and Progression of Alzheimer's Disease and Related Dementias: A Roadmap for Future Research

Author

Gordon, Marcia N, Heneka, Michael T, Le Page, Lydia M, Limberger, Christian, Morgan, David, Tenner, Andrea J, Terrando, Niccolò, Willette, Auriel A, and Willette, Sara A

Subjects
Biomedical and Clinical Sciences, Biological Psychology, Clinical Sciences, Neurosciences, Psychology, Acquired Cognitive Impairment, Infectious Diseases, Clinical Research, Neurodegenerative, Brain Disorders, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Aging, Coronaviruses, Emerging Infectious Diseases, Social Determinants of Health, Dementia, Behavioral and Social Science, Alzheimer's Disease, Coronaviruses Disparities and At-Risk Populations, 2.1 Biological and endogenous factors, Neurological, Good Health and Well Being, Alzheimer Disease, COVID-19, Caregivers, Cognitive Dysfunction, Communicable Disease Control, Humans, Alzheimer's risk factor, caregiver burden, delerium, longitudinal cohort, systemic inflammation, SARS-CoV-2, Geriatrics, Clinical sciences, Biological psychology
Abstract

COVID-19 causes lasting neurological symptoms in some survivors. Like other infections, COVID-19 may increase risk of cognitive impairment. This perspective highlights four knowledge gaps about COVID-19 that need to be filled to avoid this possible health issue. The first is the need to identify the COVID-19 symptoms, genetic polymorphisms and treatment decisions associated with risk of cognitive impairment. The second is the absence of model systems in which to test hypotheses relating infection to cognition. The third is the need for consortia for studying both existing and new longitudinal cohorts in which to monitor long term consequences of COVID-19 infection. A final knowledge gap discussed is the impact of the isolation and lack of social services brought about by quarantine/lockdowns on people living with dementia and their caregivers. Research into these areas may lead to interventions that reduce the overall risk of cognitive decline for COVID-19 survivors.

Published
2022

5. Perioperative Neurocognitive Disorder: State of the Preclinical Science.

Author

Terrando, Niccolò, Orser, Beverley, Eckenhoff, Maryellen, Eckenhoff, Roderic, Xie, Zhongcong, Culley, Deborah, Goodlin, Sarah, Zuo, Zhiyi, Wei, Huafeng, Maze, Mervyn, and Whittington, Robert

Subjects
Animals, Disease Models, Animal, Neurocognitive Disorders, Perioperative Period, Postoperative Complications, Research Design
Abstract

The purpose of this article is to provide a succinct summary of the different experimental approaches that have been used in preclinical postoperative cognitive dysfunction research, and an overview of the knowledge that has accrued. This is not intended to be a comprehensive review, but rather is intended to highlight how the many different approaches have contributed to our understanding of postoperative cognitive dysfunction, and to identify knowledge gaps to be filled by further research. The authors have organized this report by the level of experimental and systems complexity, starting with molecular and cellular approaches, then moving to intact invertebrates and vertebrate animal models. In addition, the authors goal is to improve the quality and consistency of postoperative cognitive dysfunction and perioperative neurocognitive disorder research by promoting optimal study design, enhanced transparency, and best practices in experimental design and reporting to increase the likelihood of corroborating results. Thus, the authors conclude with general guidelines for designing, conducting and reporting perioperative neurocognitive disorder rodent research.

Published
2020

6. Perioperative Neurocognitive Disorder: State of the Preclinical Science.

Author

Eckenhoff, Roderic G, Maze, Mervyn, Xie, Zhongcong, Culley, Deborah J, Goodlin, Sarah J, Zuo, Zhiyi, Wei, Huafeng, Whittington, Robert A, Terrando, Niccolò, Orser, Beverley A, and Eckenhoff, Maryellen F

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Behavioral and Social Science, Neurosciences, Animals, Disease Models, Animal, Neurocognitive Disorders, Perioperative Period, Postoperative Complications, Research Design, Anesthesiology, Clinical sciences
Abstract

The purpose of this article is to provide a succinct summary of the different experimental approaches that have been used in preclinical postoperative cognitive dysfunction research, and an overview of the knowledge that has accrued. This is not intended to be a comprehensive review, but rather is intended to highlight how the many different approaches have contributed to our understanding of postoperative cognitive dysfunction, and to identify knowledge gaps to be filled by further research. The authors have organized this report by the level of experimental and systems complexity, starting with molecular and cellular approaches, then moving to intact invertebrates and vertebrate animal models. In addition, the authors' goal is to improve the quality and consistency of postoperative cognitive dysfunction and perioperative neurocognitive disorder research by promoting optimal study design, enhanced transparency, and "best practices" in experimental design and reporting to increase the likelihood of corroborating results. Thus, the authors conclude with general guidelines for designing, conducting and reporting perioperative neurocognitive disorder rodent research.

Published
2020

8. Infection and inflammation: New perspectives on Alzheimer's disease

Author

Aiello, Alison, Chiba-Falek, Ornit, Heitman, Joseph, Johnson, Kim G., Luftig, Micah, Moseman, Ashley, Rawls, Jonathan, Shinohara, Mari L., Swanstrom, Ronald, Terrando, Niccolo, Whitson, Heather E., Colton, Carol, El Khoury, Joseph, Gate, David, Goate, Alison, Heneka, Michael T., Kaddurah-Daouk, Rima, Klein, Robyn S., Sisodia, Sangram, Spudich, Serena S., Stevens, Beth, Tanzi, Rudolph, Ting, Jenny P., and Garden, Gwenn

Published
2022
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9. 18F-florbetapir Positron Emission Tomography–determined Cerebral &bgr;-Amyloid Deposition and Neurocognitive Performance after Cardiac Surgery

Author

Klinger, Rebecca Y, James, Olga G, Borges-Neto, Salvador, Bisanar, Tiffany, Li, Yi-Ju, Qi, Wenjing, Berger, Miles, Terrando, Niccolò, Newman, Mark F, Doraiswamy, P Murali, Mathew, Joseph P, Weiner, Michael W, Aisen, Paul, Weiner, Michael, Petersen, Ronald, Jack, Clifford R, Jagust, William, Trojanowki, John Q, Toga, Arthur W, Beckett, Laurel, Green, Robert C, Saykin, Andrew J, Morris, John, Shaw, Leslie M, Khachaturian, Zaven, Sorensen, Greg, Carrillo, Maria, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, David, Mesulam, M Marcel, Potter, William, Snyder, Peter, Schwartz, Adam, Montine, Tom, Thomas, Ronald G, Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Balasubramanian, Archana B, Mason, Jennifer, Sim, Iris, Harvey, Danielle, Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, DeCArli, Charles, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Koeppe, Robert A, Foster, Norm, Reiman, Eric M, Chen, Kewei, Mathis, Chet, Landau, Susan, Morris, John C, Cairns, Louis Nigel J, Franklin, Erin, Taylor-Reinwald, Lisa, Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Crawford, Karen, Neu, Scott, Foroud, Tatiana M, Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Thal, Lean, Thal, Leon, and Buckholtz, Neil

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Brain Disorders, Neurodegenerative, Behavioral and Social Science, Dementia, Neurosciences, Acquired Cognitive Impairment, Biomedical Imaging, Clinical Research, Aging, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Alzheimer's Disease, Mental Health, 2.1 Biological and endogenous factors, Neurological, Aged, Amyloid beta-Peptides, Aniline Compounds, Brain, Cardiac Surgical Procedures, Cognitive Dysfunction, Ethylene Glycols, Female, Fluorine Radioisotopes, Humans, Male, Mental Status and Dementia Tests, Middle Aged, Positron-Emission Tomography, Postoperative Complications, Prospective Studies, Alzheimer’s Disease Neuroimaging Initiative (ADNI) Study Group, Neurologic Outcomes Research Group, Anesthesiology, Clinical sciences
Abstract

BackgroundAmyloid deposition is a potential contributor to postoperative cognitive dysfunction. The authors hypothesized that 6-week global cortical amyloid burden, determined by F-florbetapir positron emission tomography, would be greater in those patients manifesting cognitive dysfunction at 6 weeks postoperatively.MethodsAmyloid deposition was evaluated in cardiac surgical patients at 6 weeks (n = 40) and 1 yr (n = 12); neurocognitive function was assessed at baseline (n = 40), 6 weeks (n = 37), 1 yr (n = 13), and 3 yr (n = 9). The association of 6-week amyloid deposition with cognitive dysfunction was assessed by multivariable regression, accounting for age, years of education, and baseline cognition. Differences between the surgical cohort with cognitive deficit and the Alzheimer's Disease Neuroimaging Initiative cohorts (normal and early/late mild cognitive impairment) was assessed, adjusting for age, education, and apolipoprotein E4 genotype.ResultsThe authors found that 6-week abnormal global cortical amyloid deposition was not associated with cognitive dysfunction (13 of 37, 35%) at 6 weeks postoperatively (median standard uptake value ratio [interquartile range]: cognitive dysfunction 0.92 [0.89 to 1.07] vs. 0.98 [0.93 to 1.05]; P = 0.455). In post hoc analyses, global cortical amyloid was also not associated with cognitive dysfunction at 1 or 3 yr postoperatively. Amyloid deposition at 6 weeks in the surgical cohort was not different from that in normal Alzheimer's Disease Neuroimaging Initiative subjects, but increased over 1 yr in many areas at a rate greater than in controls.ConclusionsIn this study, postoperative cognitive dysfunction was not associated with 6-week cortical amyloid deposition. The relationship between cognitive dysfunction and regional amyloid burden and the rate of postoperative amyloid deposition merit further investigation.

Published
2018

10. The immune response of the human brain to abdominal surgery.

Author

Forsberg, Anton, Cervenka, Simon, Jonsson Fagerlund, Malin, Rasmussen, Lars S, Zetterberg, Henrik, Erlandsson Harris, Helena, Stridh, Pernilla, Christensson, Eva, Granström, Anna, Schening, Anna, Dymmel, Karin, Knave, Nina, Terrando, Niccolò, Maze, Mervyn, Borg, Jacqueline, Varrone, Andrea, Halldin, Christer, Blennow, Kaj, Farde, Lars, and Eriksson, Lars I

Subjects
Abdomen, Brain, Humans, Positron-Emission Tomography, Prostatectomy, Follow-Up Studies, Down-Regulation, Aged, Middle Aged, Male, Gray Matter, Biomarkers, Cognitive Dysfunction, Neurology & Neurosurgery, Clinical Sciences, Neurosciences
Abstract

ObjectiveSurgery launches a systemic inflammatory reaction that reaches the brain and associates with immune activation and cognitive decline. Although preclinical studies have in part described this systemic-to-brain signaling pathway, we lack information on how these changes appear in humans. This study examines the short- and long-term impact of abdominal surgery on the human brain immune system by positron emission tomography (PET) in relation to blood immune reactivity, plasma inflammatory biomarkers, and cognitive function.MethodsEight males undergoing prostatectomy under general anesthesia were included. Prior to surgery (baseline), at postoperative days 3 to 4, and after 3 months, patients were examined using [11 C]PBR28 brain PET imaging to assess brain immune cell activation. Concurrently, systemic inflammatory biomarkers, ex vivo blood tests on immunoreactivity to lipopolysaccharide (LPS) stimulation, and cognitive function were assessed.ResultsPatients showed a global downregulation of gray matter [11 C]PBR28 binding of 26 ± 26% (mean ± standard deviation) at 3 to 4 days postoperatively compared to baseline (p = 0.023), recovering or even increasing after 3 months. LPS-induced release of the proinflammatory marker tumor necrosis factor-α in blood displayed a reduction (41 ± 39%) on the 3rd to 4th postoperative day, corresponding to changes in [11 C]PBR28 distribution volume. Change in Stroop Color-Word Test performance between postoperative days 3 to 4 and 3 months correlated to change in [11 C]PBR28 binding (p = 0.027).InterpretationThis study translates preclinical data on changes in the brain immune system after surgery to humans, and suggests an interplay between the human brain and the inflammatory response of the peripheral innate immune system. These findings may be related to postsurgical impairments of cognitive function. Ann Neurol 2017;81:572-582.

Published
2017

18. Recommendations for the nomenclature of cognitive change associated with anaesthesia and surgery—2018

Author

Evered, Lisbeth, Eckenhoff, Roderic G., Ames, David, Bekker, Alex, Berger, Miles, Blacker, Deborah, Browndyke, Jeffrey, Crosby, Greg, Deiner, Stacie G., van Dijk, Diederik, DeKosky, Steven T., Eckenhoff, Maryellen F., Eriksson, Lars, Galasko, Dougas, Hogan, Kirk, Inouye, Sharon, Knopman, David, Lyketsos, Constantine, Marcantonio, Edward, Maruff, Paul, Maze, Mervyn, Oh, Esther, Orser, Beverley A., Ottens, Thomas, Price, Catherine, Rasmussen, Lars S., Sachdev, Perminder, Schenning, Katie, Scott, David A., Seiber, Frederick E., Silbert, Brendan, Silverstein, Jeff, Steinmetz, Jacob, Terrando, Niccolo, Trzapacz, Paula, Whittington, Rob, Xie, Zhongcong, Evered, L., Silbert, B., Knopman, D.S., Scott, D.A., DeKosky, S.T., Rasmussen, L.S., Oh, E.S., Crosby, G., Berger, M., and Eckenhoff, R.G.

Published
2018
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20. Stimulation of the α7 Nicotinic Acetylcholine Receptor Protects against Neuroinflammation after Tibia Fracture and Endotoxemia in Mice

Author

Terrando, Niccolò, Yang, Ting, Ryu, Jae Kyu, Newton, Phillip T, Monaco, Claudia, Feldmann, Marc, Ma, Daqing, Akassoglou, Katerina, and Maze, Mervyn

Subjects
Medicinal and Biomolecular Chemistry, Chemical Sciences, Neurosciences, Infectious Diseases, Patient Safety, Brain Disorders, 2.1 Biological and endogenous factors, Aetiology, Animals, Antigens, CD, Antigens, Differentiation, Myelomonocytic, Aza Compounds, CD11b Antigen, Cell Line, Cells, Cultured, Cholinergic Agonists, Cognition Disorders, Cytokines, Dioxins, Endotoxemia, Fractures, Bone, Hippocampus, Lipopolysaccharides, Macrophages, Male, Memory, Mice, Inbred C57BL, NF-kappa B, Postoperative Complications, Rats, Tibia, alpha7 Nicotinic Acetylcholine Receptor, Biochemistry and Cell Biology, Immunology, Medicinal and biomolecular chemistry
Abstract

Surgery and critical illness often associate with cognitive decline. Surgical trauma or infection can lead independently to learning and memory impairments via similar, but not identical, cellular signaling of the innate immune system that promotes neuroinflammation. In this study we explored the putative synergism between aseptic orthopedic surgery and infection, the latter reproduced by postoperative lipopolysaccharide (LPS) administration. We observed that surgery and LPS augmented systemic inflammation up to postoperative d 3 and this was associated with further neuroinflammation (CD11b and CD68 immunoreactivity) in the hippocampus in mice compared with those receiving surgery or LPS alone. Administration of a selective α7 subtype nicotinic acetylcholine receptor (α7 nAChR) agonist 2 h after LPS significantly improved neuroinflammation and hippocampal-dependent memory dysfunction. Modulation of nuclear factor-kappa B (NF-κB) activation in monocytes and regulation of the oxidative stress response through nicotinamide adenine dinucleotide phosphate (NADPH) signaling appear to be key targets in modulating this response. Overall, these results suggest that it may be conceivable to limit and possibly prevent postoperative complications, including cognitive decline and/or infections, through stimulation of the cholinergic antiinflammatory pathway.

Published
2014

21. Surgery Results in Exaggerated and Persistent Cognitive Decline in a Rat Model of the Metabolic Syndrome

Author

Feng, Xiaomei, Degos, Vincent, Koch, Lauren G, Britton, Steven L, Zhu, Yinggang, Vacas, Susana, Terrando, Niccolò, Nelson, Jeffrey, Su, Xiao, and Maze, Mervyn

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Behavioral and Social Science, Obesity, Rehabilitation, Aging, Acquired Cognitive Impairment, Cardiovascular, Brain Disorders, Nutrition, Aetiology, 2.1 Biological and endogenous factors, Analysis of Variance, Anesthesia, General, Animals, Cognition Disorders, Conditioning, Psychological, Cues, Fear, Immunity, Inflammation, Male, Maze Learning, Memory, Long-Term, Metabolic Syndrome, Motor Activity, Postoperative Complications, Rats, Running, Space Perception, Swimming, Tibial Fractures, Anesthesiology, Clinical sciences
Abstract

BackgroundPostoperative cognitive decline can be reproduced in animal models. In a well-validated rat model of the Metabolic Syndrome, we sought to investigate whether surgery induced a more severe and persistent form of cognitive decline similar to that noted in preliminary clinical studies.MethodsIn rats that had been selectively bred for low and high exercise endurance, the low capacity runners (LCR) exhibited features of Metabolic Syndrome (obesity, dyslipidemia, insulin resistance, and hypertension). Tibial fracture surgery was performed under isoflurane anesthesia in LCR and high capacity runner (HCR) rats and cognitive function was assessed postoperatively in a trace-fear conditioning paradigm and Morris Water Maze; non-operated rats were exposed to anesthesia and analgesia (sham). Group sizes were n = 6.ResultsOn postoperative D7, LCR rats had shorter freezing times than postoperative HCR rats. Five months postoperatively, LCR rats had a flatter learning trajectory and took longer to locate the submerged platform than postoperative HCR rats; dwell-time in the target quadrant in a probe trial was shorter in the postoperative LCR compared to HCR rats. LCR and HCR sham rats did not differ in any test.ConclusionPostoperatively, LCR rats diverged from HCR rats exhibiting a greater decline in memory, acutely, with persistent learning and memory decline, remotely; this could not be attributed to changes in locomotor or swimming performance. This Metabolic Syndrome animal model of surgery-induced cognitive decline corroborates, with high fidelity, preliminary findings of postoperative cognitive dysfunction in Metabolic Syndrome patients.

Published
2013

22. Inflammatory signalling in postoperative cognitive dysfunctions

Author

Terrando, Niccolò, Maze, Mervyn, and Foxwell, Brian

Subjects
617
Abstract

Major surgeries, such as cardiac or orthopaedic procedures in particular, expose the patient to extensive trauma, blood loss, and tissue injury; all of these factors effectively modulate the immune system to ultimately trigger an inflammatory response. Postoperative cognitive dysfunction (POCD), the condition being characterized by impairment of short and long-term memory, is one of common complicates following surgery. Recently, our data have demonstrated that neuroinflammation and microglia activation in the hippocampus following surgery are associated with cognitive decline. The aim of this thesis is to investigate the inflammatory signaling pathways specifically involved with POCD, with a particular interest between systemic inflammation and local inflammation in the brain following surgery. The data presented in this thesis introduce the general concepts and the involvement of inflammation in the etiology of cognitive dysfunctions using a mouse model of POCD. Upon the identification of specific pro-inflammatory markers both systemically and centrally and the delineation of the time course of events that characterize the inflammatory response following aseptic orthopaedic surgery, I describe how specific cellular signal pathways interact, mediate, and sustain this response. Following an initial non-specific approach using a general anti-inflammatory compound to identify whether inflammation plays a role in this scenario, I have exploited this model into a wide range of knockouts animals in the attempt of identifying specific signaling mechanisms and upstream receptors that mediate the behavioral abnormality following surgery. In order to achieve this, I have compared the inflammatory events after aseptic surgery with the response after a defined infectious stimulus, to ultimately joint the two in the context of a postoperative complication. In conclusion, inflammation clearly plays a pivotal role in mediating physiological as well as behavioral changes after surgery and infection. This thesis has started to unmask the signaling pathways involved with surgery and how anti-cytokine therapy can potentially ameliorate the associated cognitive dysfunction.

Published
2010
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23. The impact of IL-1 modulation on the development of lipopolysaccharide-induced cognitive dysfunction

Author

Terrando, Niccolò, Rei Fidalgo, António, Vizcaychipi, Marcela, Cibelli, Mario, Ma, Daqing, Monaco, Claudia, Feldmann, Marc, and Maze, Mervyn

Abstract

Abstract Introduction The impact of pro-inflammatory cytokines on neuroinflammation and cognitive function after lipopolysaccharide (LPS) challenge remains elusive. Herein we provide evidence that there is a temporal correlation between high-mobility group box 1 (HMGB-1), microglial activation, and cognitive dysfunction. Disabling the interleukin (IL)-1 signaling pathway is sufficient to reduce inflammation and ameliorate the disability. Methods Endotoxemia was induced in wild-type and IL-1R-/- mice by intra peritoneal injection of E. Coli LPS (1 mg/kg). Markers of inflammation were assessed both peripherally and centrally, and correlated to behavioral outcome using trace fear conditioning. Results Increase in plasma tumor necrosis factor-α (TNFα) peaked at 30 minutes after LPS challenge. Up-regulation of IL-1β, IL-6 and HMGB-1 was more persistent, with detectable levels up to day three. A 15-fold increase in IL-6 and a 6.5-fold increase in IL-1β mRNA at 6 hours post intervention (P < 0.001 respectively) was found in the hippocampus. Reactive microgliosis was observed both at days one and three, and was associated with elevated HMGB-1 and impaired memory retention (P < 0.005). Preemptive administration of IL-1 receptor antagonist (IL-1Ra) significantly reduced plasma cytokines and hippocampal microgliosis and ameliorated cognitive dysfunction without affecting HMGB-1 levels. Similar results were observed in LPS-challenged mice lacking the IL-1 receptor to those seen in LPS-challenged wild type mice treated with IL-1Ra. Conclusions These data suggest that by blocking IL-1 signaling, the inflammatory cascade to LPS is attenuated, thereby reducing microglial activation and preventing the behavioral abnormality.

Published
2010

29. Intravenous Lidocaine Does Not Improve Neurologic Outcomes after Cardiac Surgery: A Randomized Controlled Trial

Author

Klinger, Rebecca Y., Cooter, Mary, Bisanar, Tiffany, Terrando, Niccolò, Berger, Miles, Podgoreanu, Mihai V., Stafford-Smith, Mark, Newman, Mark F., Mathew, Joseph P., Blumenthal, James A., Karhausen, Jorn A., Kertai, Miklos D., Krishnamoorthy, Vijay, Li, Yi-Ju, Swaminathan, Madhav, Warner, David S., Funk, Bonita L., Brassard, Rachele, Toulgoat-Dubois, Yanne, Waweru, Peter, Babyak, Michael A., Blumenthal, James A., Browndyke, Jeffrey N., Welsh-Bohmer, Kathleen A., Sketch, Michael H., Jr., Bennett, Ellen R., Graffagnino, Carmelo, Laskowitz, Daniel T., Strittmatter, Warren J., Collins, Kevin, Smigla, Greg, Shearer, Ian, D’Amico, Thomas A., Daneshmand, Mani A., Gaca, Jeffrey G., Glower, Donald D., Haney, Jack, Harpole, David, Hartwig, Mathew G., Hughes, G. Chad, Klapper, Jacob A., Lin, Shu S., Lodge, Andrew J., Milano, Carmelo A., Plichta, Ryan P., Schroeder, Jacob N., Smith, Peter K., and Tong, Betty C.

Published
2019
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32. Role of Blood–Brain Barrier Dysfunction in Delirium following Non‐cardiac Surgery in Older Adults.

Author

Devinney, Michael J., Wong, Megan K., Wright, Mary Cooter, Marcantonio, Edward R., Terrando, Niccolò, Browndyke, Jeffrey N., Whitson, Heather E., Cohen, Harvey J., Nackley, Andrea G., Klein, Marguerita E., Ely, E. Wesley, Mathew, Joseph P., and Berger, Miles

Subjects
BLOOD-brain barrier, OLDER people, DELIRIUM, LENGTH of stay in hospitals, CEREBROSPINAL fluid, BLOOD sampling
Abstract

Objective: Although animal models suggest a role for blood–brain barrier dysfunction in postoperative delirium‐like behavior, its role in postoperative delirium and postoperative recovery in humans is unclear. Thus, we evaluated the role of blood–brain barrier dysfunction in postoperative delirium and hospital length of stay among older surgery patients. Methods: Cognitive testing, delirium assessment, and cerebrospinal fluid and blood sampling were prospectively performed before and after non‐cardiac, non‐neurologic surgery. Blood–brain barrier dysfunction was assessed using the cerebrospinal fluid‐to‐plasma albumin ratio (CPAR). Results: Of 207 patients (median age = 68 years, 45% female) with complete CPAR and delirium data, 26 (12.6%) developed postoperative delirium. Overall, CPAR increased from before to 24 hours after surgery (median change = 0.28, interquartile range [IQR] = −0.48 to 1.24, Wilcoxon p = 0.001). Preoperative to 24 hours postoperative change in CPAR was greater among patients who developed delirium versus those who did not (median [IQR] = 1.31 [0.004 to 2.34] vs 0.19 [−0.55 to 1.08], p = 0.003). In a multivariable model adjusting for age, baseline cognition, and surgery type, preoperative to 24 hours postoperative change in CPAR was independently associated with delirium occurrence (per CPAR increase of 1, odds ratio = 1.30, 95% confidence interval [CI] = 1.03–1.63, p = 0.026) and increased hospital length of stay (incidence rate ratio = 1.15, 95% CI = 1.09–1.22, p < 0.001). Interpretation: Postoperative increases in blood–brain barrier permeability are independently associated with increased delirium rates and postoperative hospital length of stay. Although these findings do not establish causality, studies are warranted to determine whether interventions to reduce postoperative blood–brain barrier dysfunction would reduce postoperative delirium rates and hospital length of stay. ANN NEUROL 2023;94:1024–1035 [ABSTRACT FROM AUTHOR]

Published
2023
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38. 18F-florbetapir Positron Emission Tomography–determined Cerebral β-Amyloid Deposition and Neurocognitive Performance after Cardiac Surgery

Author

Klinger, Rebecca Y., James, Olga G., Borges-Neto, Salvador, Bisanar, Tiffany, Li, Yi-Ju, Qi, Wenjing, Berger, Miles, Terrando, Niccolò, Newman, Mark F., Doraiswamy, P. Murali, Mathew, Joseph P., Weiner, Michael W., Aisen, Paul, Weiner, Michael, Aisen, Paul, Petersen, Ronald, Jack, Clifford R., Jr., Jagust, William, Trojanowki, John Q., Toga, Arthur W., Beckett, Laurel, Green, Robert C., Saykin, Andrew J., Morris, John, Shaw, Leslie M., Khachaturian, Zaven, Sorensen, Greg, Carrillo, Maria, Kuller, Lew, Raichle, Marc, Paul, Steven, Davies, Peter, Fillit, Howard, Hefti, Franz, Holtzman, David, Mesulam, M. Marcel, Potter, William, Snyder, Peter, Schwartz, Adam, Green, Robert C., Montine, Tom, Petersen, Ronald, Aisen, Paul, Thomas, Ronald G., Donohue, Michael, Walter, Sarah, Gessert, Devon, Sather, Tamie, Jiminez, Gus, Balasubramanian, Archana B., Mason, Jennifer, Sim, Iris, Beckett, Laurel, Harvey, Danielle, Donohue, Michael, Jack, Clifford R., Jr., Bernstein, Matthew, Fox, Nick, Thompson, Paul, Schuff, Norbert, DeCArli, Charles, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Vemuri, Prashanthi, Jones, David, Kantarci, Kejal, Ward, Chad, Jagust, William, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Mathis, Chet, Landau, Susan, Morris, John C., Cairns, Louis Nigel J., Franklin, Erin, Taylor-Reinwald, Lisa, Shaw, Leslie M., Trojanowki, John Q., Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Toga, Arthur W., Crawford, Karen, Neu, Scott, Saykin, Andrew J., Foroud, Tatiana M., Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Weiner, Michael W., Thal, Lean, Khachaturian, Zaven, Thal, Leon, Buckholtz, Neil, Weiner, Michael W., Snyder, Peter J., Potter, William, Paul, Steven, Albert, Marilyn, Frank, Richard, Khachaturian, Zaven, Hsiao, John, Kaye, Jeffrey, Quinn, Joseph, Silbert, Lisa, Lind, Betty, Carter, Raina, Dolen, Sara, Schneider, Lon S., Pawluczyk, Sonia, Becerra, Mauricio, Teodoro, Liberty, Spann, Bryan M., Brewer, James, Vanderswag, Helen, Fleisher, Adam, Heidebrink, Judith L., Lord, Joanne L., Petersen, Ronald, Mason, Sara S., Albers, Colleen S., Knopman, David, Johnson, Kris, Doody, Rachelle S., Villanueva-Meyer, Javier, Pavlik, Valory, Shibley, Victoria, Chowdhury, Munir, Rountree, Susan, Dang, Mimi, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Ances, Beau, Morris, John C., Carroll, Maria, Creech, Mary L., Franklin, Erin, Mintun, Mark A., Schneider, Stacy, Oliver, Angela, Marson, Daniel, Geldmacher, David, Love, Marissa Natelson, Griffith, Randall, Clark, David, Brockington, John, Roberson, Erik, Grossman, Hillel, Mitsis, Effie, Shah, Raj C., deToledo-Morrell, Leyla, Duara, Ranjan, Greig-Custo, Maria T., Barker, Warren, Albert, Marilyn, Onyike, Chiadi, D’Agostino, Daniel, II, Kielb, Stephanie, Sadowski, Martin, Sheikh, Mohammed O., Ulysse, Anaztasia, Gaikwad, Mrunalini, Petrella, Jeffrey R., Wong, Terence Z., Coleman, Edward, Arnold, Steven E., Karlawish, Jason H., Wolk, David A., Clark, Christopher M., Smith, Charles D., Jicha, Greg, Hardy, Peter, Sinha, Partha, Oates, Elizabeth, Conrad, Gary, Lopez, Oscar L., Oakley, MaryAnn, Simpson, Donna M., Porsteinsson, Anton P., Goldstein, Bonnie S., Martin, Kim, Makino, Kelly M., Ismail, M. Saleem, Brand, Connie, Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Womack, Kyle, Mathews, Dana, Quiceno, Mary, Levey, Allan I., Lah, James J., Cellar, Janet S., Burns, Jeffrey M., Swerdlow, Russell H., Brooks, William M., Apostolova, Liana, Tingus, Kathleen, Woo, Ellen, Silverman, Daniel H.S., Lu, Po H., Bartzokis, George, Graff-Radford, Neill R, Parfitt, Francine, Poki-Walker, Kim, Farlow, Martin R., Hake, Ann Marie, Matthews, Brandy R., Brosch, Jared R., Herring, Scott, van Dyck, Christopher H., Carson, Richard E., MacAvoy, Martha G., Varma, Pradeep, Chertkow, Howard, Bergman, Howard, Hosein, Chris, Black, Sandra, Stefanovic, Bojana, Caldwell, Curtis, Ging-Yuek, Hsiung, Robin, Mudge, Benita, Sossi, Vesna, Feldman, Howard, Assaly, Michele, Finger, Elizabeth, Pasternack, Stephen, Rachisky, Irina, Trost, Dick, Kertesz, Andrew, Bernick, Charles, Munic, Donna, Mesulam, Marek-Marsel, Rogalski, Emily, Lipowski, Kristine, Weintraub, Sandra, Bonakdarpour, Borna, Kerwin, Diana, Wu, Chuang-Kuo, Johnson, Nancy, Sadowsky, Carl, Villena, Teresa, Turner, Raymond Scott, Johnson, Kathleen, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Yesavage, Jerome, Taylor, Joy L., Lane, Barton, Rosen, Allyson, Tinklenberg, Jared, Sabbagh, Marwan N., Belden, Christine M., Jacobson, Sandra A., Sirrel, Sherye A., Kowall, Neil, Killiany, Ronald, Budson, Andrew E., Norbash, Alexander, Johnson, Patricia Lynn, Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Lerner, Alan, Ogrocki, Paula, Tatsuoka, Curtis, Fatica, Parianne, Fletcher, Evan, Maillard, Pauline, Olichney, John, DeCarli, Charles, Carmichael, Owen, Kittur, Smita, Borrie, Michael, Lee, T-Y, Bartha, Dr Rob, Johnson, Sterling, Asthana, Sanjay, Carlsson, Cynthia M., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Tariot, Pierre, Burke, Anna, Milliken, Ann Marie, Trncic, Nadira, Fleisher, Adam, Reeder, Stephanie, Bates, Vernice, Capote, Horacio, Rainka, Michelle, Scharre, Douglas W., Kataki, Maria, Kelley, Brendan, Zimmerman, Earl A., Celmins, Dzintra, Brown, Alice D., Pearlson, Godfrey D., Blank, Karen, Anderson, Karen, Flashman, Laura A., Seltzer, Marc, Hynes, Mary L., Santulli, Robert B., Sink, Kaycee M., Gordineer, Leslie, Williamson, Jeff D., Garg, Pradeep, Watkins, Franklin, Ott, Brian R., Tremont, Geoffrey, Daiello, Lori A., Salloway, Stephen, Malloy, Paul, Correia, Stephen, Rosen, Howard J., Miller, Bruce L., Perry, David, Mintzer, Jacobo, Spicer, Kenneth, Bachman, David, Finger, Elizabeth, Pasternak, Stephen, Rachinsky, Irina, Rogers, John, Kertesz, Andrew, Drost, Dick, Pomara, Nunzio, Hernando, Raymundo, Sarrael, Antero, Schultz, Susan K., Smith, Karen Ekstam, Koleva, Hristina, Nam, Ki Won, Shim, Hyungsub, Relkin, Norman, Chiang, Gloria, Lin, Michael, Ravdin, Lisa, Smith, Amanda, Ashok Raj, Balebail, Fargher, Kristin, Weiner, Michael W., Aisen, Paul, Weiner, Michael, Aisen, Paul, Petersen, Ronald, Green, Robert C., Harvey, Danielle, Jack, Clifford R., Jr., Jagust, William, Morris, John C., Saykin, Andrew J., Shaw, Leslie M., Toga, Arthur W., Trojanowki, John Q., Neylan, Thomas, Grafman, Jordan, Grafman, Jordan, Green, Robert C., Montine, Tom, Weiner, Michael, Petersen, Ronald, Aisen, Paul, Thomas, Ronald G., Donohue, Michael, Gessert, Devon, Sather, Tamie, Davis, Melissa, Morrison, Rosemary, Jiminez, Gus, Neylan, Thomas, Hayes, Jacqueline, Finely, Shannon, Harvey, Danielle, Donohue, Michael, Jack, Clifford R., Jr., Bernstein, Matthew, Borowski, Bret, Gunter, Jeff, Senjem, Matt, Kantarci, Kejal, Ward, Chad, Jagust, William, Koeppe, Robert A., Foster, Norm, Reiman, Eric M., Chen, Kewei, Landau, Susan, Morris, John C., Cairns, Nigel J., Householder, Erin, Shaw, Leslie M., Trojanowki, John Q., Lee, Virginia, Korecka, Magdalena, Figurski, Michal, Toga, Arthur W., Crawford, Karen, Neu, Scott, Saykin, Andrew J., Foroud, Tatiana M., Potkin, Steven, Shen, Li, Faber, Kelley, Kim, Sungeun, Nho, Kwangsik, Weiner, Michael W., Friedl, Karl, Schneider, Lon S., Pawluczyk, Sonia, Becerra, Mauricio, Brewer, James, Vanderswag, Helen, Stern, Yaakov, Honig, Lawrence S., Bell, Karen L., Fleischman, Debra, Arfanakis, Konstantinos, Shah, Raj C., Duara, Ranjan, Varon, Daniel, Greig, Maria T, Petrella, Jeffrey R., Porsteinsson, Anton P., Goldstein, Bonnie, Martin, Kimberly S., Potkin, Steven G., Preda, Adrian, Nguyen, Dana, Mintzer, Jacobo, Massoglia, Dino, Brawman-Mintzer, Olga, Sadowsky, Carl, Martinez, Walter, Villena, Teresa, Jagust, William, Landau, Susan, Rosen, Howard, Perry, David, Turner, Raymond Scott, Behan, Kelly, Reynolds, Brigid, Sperling, Reisa A., Johnson, Keith A., Marshall, Gad, Sabbagh, Marwan N., Jacobson, Sandra A., Sirrel, Sherye A., Obisesan, Thomas O., Wolday, Saba, Allard, Joanne, Johnson, Sterling C., Fruehling, J. Jay, Harding, Sandra, Peskind, Elaine R., Petrie, Eric C., Li, Gail, Yesavage, Jerome A., Taylor, Joy L., Furst, Ansgar J., Chao, Steven, Relkin, Norman, Chiang, Gloria, Ravdin, Lisa, Blumenthal, James A., Karhausen, Jorn A., Kertai, Miklos D., Podgoreanu, Mihai V., Stafford-Smith, Mark, Swaminathan, Madhav, Warner, David S., Funk, Bonita L., Balajonda, Narai, Brassard, Rachele, Cooter, Mary, Toulgoat-Dubois, Yanne, Waweru, Peter, Babyak, Michael A., Blumenthal, James A., Browndyke, Jeffrey N., Welsh-Bohmer, Kathleen A., Sketch, Michael H., Jr., Bennett, Ellen R., Graffagnino, Carmelo, Laskowitz, Daniel T., Strittmatter, Warren J., Collins, Kevin, Smigla, Greg, Shearer, Ian, D’Amico, Thomas A., Daneshmand, Mani A., Gaca, R. Jeffrey G., Glower, Donald D., Haney, Jack, Harpole, R. David, Hartwig, Mathew G., Hughes, G. Chad, Klapper, Jacob A., Lin, Shu S., Lodge, Andrew J., Milano, Carmelo A., Plichta, Ryan P., Schroeder, Jacob N., Smith, Peter K., and Tong, Betty C.

Published
2018
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41. Conserved YKL-40 changes in mice and humans after postoperative delirium

Author

David-Bercholz, Jennifer, primary, Acker, Leah, additional, Caceres, Ana I, additional, Wu, Pau Yen, additional, Goenka, Saanvi, additional, Franklin, Nathan O, additional, Rodriguiz, Ramona M, additional, Wetsel, William C, additional, Devinney, Michael, additional, Wright, Mary Cooter, additional, Zetterberg, Henrik, additional, Yang, Ting, additional, Berger, Miles, additional, and Terrando, Niccolò, additional

Published
2022
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42. Thinking, fast and slow: highlights from the 2016 BJA seminar on anaesthetic neurotoxicity and neuroplasticity

Author

Soriano, S. G., Vutskits, L., Jevtovic-Todorovic, V., Hemmings, H. C., Davidson, Andrew, Warner, David O, Johnson-Akeju, Oluwaseun, McCann, Mary Ellen, Ing, Caleb, Absalom, Anthony, Brambrink, Ansgar, Alvarado, Maria, Slikker, William, Jr., Fitzgerald, Maria, Mintz, C. David, Pearn, Matthew, Platholi, Jimcy, Sinner, Barbara, Soriano, Sulpicio G, Terrando, Niccolò, Walker, Suellen M, Huang, Han, Degos, Vincent, Xie, Zhongcong, Mantz, Jean, Patel, Piyush, Loepke, Andreas W., Wang, Tian-Long, Bosnjak, Zeljko, Sall, Jeffrey, Ma, Daqing, and Sun, Lena S.

Published
2017
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43. The role of peripheral inflammatory insults in Alzheimer's disease: a review and research roadmap.

Author

Walker, Keenan A., Le Page, Lydia M., Terrando, Niccolò, Duggan, Michael R., Heneka, Michael T., and Bettcher, Brianne M.

Subjects
ALZHEIMER'S disease, DISEASE risk factors, INFLAMMATION, THERAPEUTICS, EVIDENCE gaps
Abstract

Peripheral inflammation, defined as inflammation that occurs outside the central nervous system, is an age-related phenomenon that has been identified as a risk factor for Alzheimer's disease. While the role of chronic peripheral inflammation has been well characterized in the context of dementia and other age-related conditions, less is known about the neurologic contribution of acute inflammatory insults that take place outside the central nervous system. Herein, we define acute inflammatory insults as an immune challenge in the form of pathogen exposure (e.g., viral infection) or tissue damage (e.g., surgery) that causes a large, yet time-limited, inflammatory response. We provide an overview of the clinical and translational research that has examined the connection between acute inflammatory insults and Alzheimer's disease, focusing on three categories of peripheral inflammatory insults that have received considerable attention in recent years: acute infection, critical illness, and surgery. Additionally, we review immune and neurobiological mechanisms which facilitate the neural response to acute inflammation and discuss the potential role of the blood–brain barrier and other components of the neuro-immune axis in Alzheimer's disease. After highlighting the knowledge gaps in this area of research, we propose a roadmap to address methodological challenges, suboptimal study design, and paucity of transdisciplinary research efforts that have thus far limited our understanding of how pathogen- and damage-mediated inflammatory insults may contribute to Alzheimer's disease. Finally, we discuss how therapeutic approaches designed to promote the resolution of inflammation may be used following acute inflammatory insults to preserve brain health and limit progression of neurodegenerative pathology. [ABSTRACT FROM AUTHOR]

Published
2023
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47. Perioperative Cognitive Decline in the Aging Population

Author

Terrando, Niccolò, Brzezinski, Marek, Degos, Vincent, Eriksson, Lars I., Kramer, Joel H., Leung, Jacqueline M., Miller, Bruce L., Seeley, William W., Vacas, Susana, Weiner, Michael W., Yaffe, Kristine, Young, William L., Xie, Zhongcong, and Maze, Mervyn

Published
2011
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50. Preclinical and translational models for delirium: Recommendations for future research from the NIDUS delirium network.

Author

Vasunilashorn, Sarinnapha M., Lunardi, Nadia, Newman, John C., Crosby, Gregory, Acker, Leah, Abel, Ted, Bhatnagar, Seema, Cunningham, Colm, de Cabo, Rafael, Dugan, Laura, Hippensteel, Joseph A., Ishizawa, Yumiko, Lahiri, Shouri, Marcantonio, Edward R., Xie, Zhongcong, Inouye, Sharon K., Terrando, Niccolò, and Eckenhoff, Roderic G.

Abstract

Delirium is a common, morbid, and costly syndrome that is closely linked to Alzheimer's disease (AD) and AD‐related dementias (ADRD) as a risk factor and outcome. Human studies of delirium have advanced our knowledge of delirium incidence and prevalence, risk factors, biomarkers, outcomes, prevention, and management. However, understanding of delirium neurobiology remains limited. Preclinical and translational models for delirium, while challenging to develop, could advance our knowledge of delirium neurobiology and inform the development of new prevention and treatment approaches. We discuss the use of preclinical and translational animal models in delirium, focusing on (1) a review of current animal models, (2) challenges and strategies for replicating elements of human delirium in animals, and (3) the utility of biofluid, neurophysiology, and neuroimaging translational markers in animals. We conclude with recommendations for the development and validation of preclinical and translational models for delirium, with the goal of advancing awareness in this important field. [ABSTRACT FROM AUTHOR]

Published
2023
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