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Article ; Online: Early aggressive intervention might improve outcomes of postoperative mediastinitis in children.

Bohuta, Lyubomyr / McMullan, Michael D

European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery

2021 Volume 59, Issue 5, Page(s) 957–958

MeSH term(s)	Child ; Humans ; Mediastinitis ; Postoperative Complications ; Postoperative Period
Language	English
Publishing date	2021-05-04
Publishing country	Germany
Document type	Editorial ; Comment
ZDB-ID	639293-3
ISSN	1873-734X ; 1010-7940 ; 1567-4258
ISSN (online)	1873-734X
ISSN	1010-7940 ; 1567-4258
DOI	10.1093/ejcts/ezab068
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Zs.A 2303: Show issues

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Article ; Online: Baseline serum brain-derived neurotrophic factor association with future cognition in community-dwelling older adults undergoing annual memory screening.

Keegan, Andrew P / Stough, Con / Paris, Daniel / Luis, Cheryl A / Abdullah, Laila / Ait-Ghezala, Ghania / Chaykin, Jillian / Crawford, Fiona / Mullan, Michael

Neurological research

2024 Volume 46, Issue 3, Page(s) 253–260

Abstract: Objectives: It has been shown that peripheral measures of brain-derived neurotrophic factor (BNDF), an important neurotrophin instrumental to the biology of learning, may contribute to predicting cognitive decline. However, the two primary forms of BDNF, ...

Abstract	Objectives: It has been shown that peripheral measures of brain-derived neurotrophic factor (BNDF), an important neurotrophin instrumental to the biology of learning, may contribute to predicting cognitive decline. However, the two primary forms of BDNF, mature (mBDNF) and pro (proBDNF), and how they contribute to cognition longitudinally has not been well studied. Methods: Eighty-two older adults (average age 72.2 ± 6.4 years) provided blood samples at two time points separated on average by 4.2 years while participating in an annual memory screening that included the MoCA (Montreal Cognitive Assessment) and GDS (Geriatric Depression Scale). Both mBDNF and proBDNF from serum were quantified at each time point. Whole blood samples were genotyped for Results: Using logistic regression analysis controlling for age, sex, baseline MoCA score, Discussion: This study further supports that mBDNF measured in the serum of older adults may reflect a protective role while proBDNF requires further investigation.
MeSH term(s)	Humans ; Aged ; Brain-Derived Neurotrophic Factor/genetics ; Independent Living ; Cognition ; Cognitive Dysfunction/diagnosis ; Cognitive Dysfunction/genetics ; Apolipoproteins E
Chemical Substances	Brain-Derived Neurotrophic Factor ; Apolipoproteins E
Language	English
Publishing date	2024-01-22
Publishing country	England
Document type	Journal Article
ZDB-ID	424428-x
ISSN	1743-1328 ; 0161-6412
ISSN (online)	1743-1328
ISSN	0161-6412
DOI	10.1080/01616412.2023.2294581
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Zs.A 1491: Show issues

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Article ; Online: ApoE4 expression disrupts tau uptake, trafficking, and clearance in astrocytes.

Eisenbaum, Maxwell / Pearson, Andrew / Ortiz, Camila / Mullan, Michael / Crawford, Fiona / Ojo, Joseph / Bachmeier, Corbin

Glia

2023 Volume 72, Issue 1, Page(s) 184–205

Abstract: Tauopathies are a collection of neurodegenerative diseases characterized by the accumulation of pathogenic aggregates of the microtubule-associated protein tau. Despite the prevalence and diversity of tau astrogliopathy in tauopathies, the interactions ... ...

Abstract	Tauopathies are a collection of neurodegenerative diseases characterized by the accumulation of pathogenic aggregates of the microtubule-associated protein tau. Despite the prevalence and diversity of tau astrogliopathy in tauopathies, the interactions between astrocytes and tau in the brain, and the influence of neurodegenerative genetic risk factors like the apolipoprotein E4 (apoE4) isoform, are largely unknown. Here, we leveraged primary and immortalized astrocytes expressing humanized apoE isoforms to characterize the mechanisms by which astrocytes interact with and eliminate extracellular tau, and the influence of apoE genotype on these processes. Our work indicates that astrocytes rapidly internalize, process, and release tau via an exosomal secretory mechanism under physiological conditions. However, we found that apoE4 disrupted these processes in comparison to apoE3, resulting in an astrocytic phenotype prone to intracellular tau accumulation. Furthermore, exposure to repetitive mild traumatic brain injuries exacerbated the apoE4-induced impairments in tau processing and elimination by astrocytes in apoE4 targeted-replacement mice. The diminished ability of apoE4 astrocytes to eliminate extracellular tau can lead to an accumulation of pathogenic tau, which induces mitochondrial dysfunction, as demonstrated by our studies. In total, our findings suggest that the apoE4 isoform lowers the threshold of astrocytic resilience to pathogenic tau, rendering them susceptible to bioenergetic deficits in the early stages of neurodegenerative diseases such as traumatic brain injury, potentially contributing to neurological decline.
MeSH term(s)	Mice ; Animals ; Apolipoprotein E4/genetics ; Astrocytes/metabolism ; Mice, Transgenic ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Tauopathies/pathology ; Neurodegenerative Diseases/metabolism ; Protein Isoforms/genetics ; Protein Isoforms/metabolism
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E ; Protein Isoforms
Language	English
Publishing date	2023-09-05
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24469
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Zs.A 2345: Show issues

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Article ; Online: Repetitive head trauma and apoE4 induce chronic cerebrovascular alterations that impair tau elimination from the brain.

Eisenbaum, Maxwell / Pearson, Andrew / Ortiz, Camila / Koprivica, Milica / Cembran, Arianna / Mullan, Michael / Crawford, Fiona / Ojo, Joseph / Bachmeier, Corbin

Experimental neurology

2024 Volume 374, Page(s) 114702

Abstract: Repetitive mild traumatic brain injuries (r-mTBI) sustained in the military or contact sports have been associated with the accumulation of extracellular tau in the brain, which may contribute to the pathogenesis of neurodegenerative tauopathies. The ... ...

Abstract	Repetitive mild traumatic brain injuries (r-mTBI) sustained in the military or contact sports have been associated with the accumulation of extracellular tau in the brain, which may contribute to the pathogenesis of neurodegenerative tauopathies. The expression of the apolipoprotein E4 (apoE4) isoform has been associated with higher levels of tau in the brain, and worse clinical outcomes after r-mTBI, though the influence of apoE genotype on extracellular tau dynamics in the brain is poorly understood. We recently demonstrated that extracellular tau can be eliminated across blood-brain barrier (BBB), which is progressively impaired following r-mTBI. The current studies investigated the influence of repetitive mild TBI (r-mTBI) and apoE genotype on the elimination of extracellular solutes from the brain. Following intracortical injection of biotin-labeled tau into humanized apoE-Tr mice, the levels of exogenous tau residing in the brain of apoE4 mice were elevated compared to other isoforms, indicating reduced tau elimination. Additionally, we found exposure to r-mTBI increased tau residence in apoE2 mice, similar to our observations in E2FAD animals. Each of these findings may be the result of diminished tau efflux via LRP1 at the BBB, as LRP1 inhibition significantly reduced tau uptake in endothelial cells and decreased tau transit across an in vitro model of the BBB (basolateral-to-apical). Notably, we showed that injury and apoE status, (particularly apoE4) resulted in chronic alterations in BBB integrity, pericyte coverage, and AQP4 polarization. These aberrations coincided with an atypical reactive astrocytic gene signature indicative of diminished CSF-ISF exchange. Our work found that CSF movement was reduced in the chronic phase following r-mTBI (>18 months post injury) across all apoE genotypes. In summary, we show that apoE genotype strongly influences cerebrovascular homeostasis, which can lead to age-dependent deficiencies in the elimination of toxic proteins from the brain, like tau, particularly in the aftermath of head trauma.
MeSH term(s)	Mice ; Animals ; Apolipoprotein E4/genetics ; Apolipoprotein E4/metabolism ; Mice, Transgenic ; Endothelial Cells/metabolism ; Brain/metabolism ; Apolipoproteins E/genetics ; Apolipoproteins E/metabolism ; Brain Concussion/metabolism
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E
Language	English
Publishing date	2024-01-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2024.114702
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Zs.A 184: Show issues

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Article ; Online: Double-Chambered Right Ventricle in Adulthood: A Case Series.

Malone, Richard Joseph / Henderson, Everett Randall / Wilson, Zachary Ryan / McMullan, Matthew R / Skelton, Thomas N / Campbell, William F / McMullan, Michael R

CASE (Philadelphia, Pa.)

2024 Volume 8, Issue 3Part A, Page(s) 202–209

Language	English
Publishing date	2024-03-08
Publishing country	United States
Document type	Case Reports
ISSN	2468-6441
ISSN (online)	2468-6441
DOI	10.1016/j.case.2023.12.012
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Article ; Online: Subacute and chronic proteomic and phosphoproteomic analyses of a mouse model of traumatic brain injury at two timepoints and comparison with chronic traumatic encephalopathy in human samples.

Morin, Alexander / Davis, Roderick / Darcey, Teresa / Mullan, Michael / Mouzon, Benoit / Crawford, Fiona

Molecular brain

2022 Volume 15, Issue 1, Page(s) 62

Abstract: Repetitive mild traumatic brain injury (r-mTBI) is the most widespread type of brain trauma worldwide. The cumulative injury effect triggers long-lasting pathological and molecular changes that may increase risk of chronic neurodegenerative diseases. R- ... ...

Abstract	Repetitive mild traumatic brain injury (r-mTBI) is the most widespread type of brain trauma worldwide. The cumulative injury effect triggers long-lasting pathological and molecular changes that may increase risk of chronic neurodegenerative diseases. R-mTBI is also characterized by changes in the brain proteome, where the majority of molecules altered early post-TBI are different from those altered at more chronic phases. This differentiation may contribute to the heterogeneity of available data on potential therapeutic targets and may present an obstacle in developing effective treatments. Here, we aimed to characterize a proteome profile of r-mTBI in a mouse model at two time points - 3 and 24 weeks post last TBI, as this may be a more relevant therapeutic window for individuals suffering negative consequences of r-mTBI. We identified a great number of proteins and phosphoproteins that remain continuously dysregulated from 3 to 24 weeks. These proteins may serve as effective therapeutic targets for sub-acute and chronic stages of post r-mTBI. We also compared canonical pathway activation associated with either total proteins or phosphoproteins and revealed that they both are upregulated at 24 weeks. However, at 3 weeks post-TBI, only pathways associated with total proteins are upregulated, while pathways driven by phosphoproteins are downregulated. Finally, to assess the translatability of our data, we compared proteomic changes in our mouse model with those reported in autopsied human samples of Chronic Traumatic Encephalopathy (CTE) patients compared to controls. We observed 39 common proteins that were upregulated in both species and 24 common pathways associated with these proteins. These findings support the translational relevance of our mouse model of r-mTBI for successful identification and translation of therapeutic targets.
MeSH term(s)	Animals ; Brain Concussion/complications ; Brain Concussion/metabolism ; Brain Concussion/pathology ; Brain Injuries, Traumatic/complications ; Chronic Disease ; Chronic Traumatic Encephalopathy/complications ; Disease Models, Animal ; Humans ; Mice ; Phosphoproteins ; Proteome ; Proteomics
Chemical Substances	Phosphoproteins ; Proteome
Language	English
Publishing date	2022-07-18
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2436057-0
ISSN	1756-6606 ; 1756-6606
ISSN (online)	1756-6606
ISSN	1756-6606
DOI	10.1186/s13041-022-00945-4
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Article ; Online: Bacopa monnieri

Keegan, Andrew P / Stough, Con / Paris, Daniel / Luis, Cheryl A / Abdullah, Laila / Ait-Ghezala, Ghania / Crawford, Fiona / Mullan, Michael

Journal of clinical and translational research

2023 Volume 9, Issue 1, Page(s) 50–58

Abstract: Background and aim: Bacopa monnieri: Methods: Bacopa was administered in an open-labeled study to cognitively healthy controls over a 3-month period. Cognition and mood were assessed using the Montreal Cognitive Assessment (MoCA) and geriatric ... ...

Abstract	Background and aim: Bacopa monnieri Methods: Bacopa was administered in an open-labeled study to cognitively healthy controls over a 3-month period. Cognition and mood were assessed using the Montreal Cognitive Assessment (MoCA) and geriatric depression scale (GDS) at the baseline and 3-month visit. Laboratories were assessed for safety and serum levels of mature (mBDNF) and proBDNF were quantified. In a subset of subjects, intracellular signaling processes were assessed using western blot analysis. Results: Bacopa was provided to 35 subjects and was well-tolerated except for 4 (11%) subjects who early terminated due to known, reversible, and gastrointestinal side effects (i.e., nausea, diarrhea). Over the 3 months, the GDS and the total MoCA did not significantly change; however, the delayed-recall subscale significantly improved (baseline: 3.8 ± 1.2, 3-months: 4.3 ± 0.9; Conclusion: These results suggest that Bacopa may exert an anti-inflammatory effect through NF-κB and improve intracellular signaling processes associated with synaptogenesis (CREB). The future placebo-controlled studies are recommended. Relevance for patients: B. monnieri
Language	English
Publishing date	2023-01-17
Publishing country	Singapore
Document type	Journal Article
ZDB-ID	3019815-X
ISSN	2424-810X ; 2382-6533
ISSN (online)	2424-810X
ISSN	2382-6533
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Article ; Online: Using Arterial Recoil for Large Bore Access Closure After Impella Assist Device Removal.

Talha, Khawaja M / Winscott, John G / Patel, Vishal / Lemor, Alejandro / Ashley, Kellan E / Campbell, William F / McMullan, Michael R / Hernandez, Gabriel A

Critical pathways in cardiology

2023 Volume 23, Issue 1, Page(s) 36–38

Abstract: The use of Impella assist device for high-risk percutaneous coronary interventions and cardiogenic shock has increased in the last decade and requires a large bore arterial access (LBA). However, LBA closure following Impella removal is associated with ... ...

Abstract	The use of Impella assist device for high-risk percutaneous coronary interventions and cardiogenic shock has increased in the last decade and requires a large bore arterial access (LBA). However, LBA closure following Impella removal is associated with significant complications. Herein, we describe the safety and efficacy of a novel method of LBA closure using arterial recoil following Impella removal. We performed a retrospective review of electronic medical records of patients who underwent LBA closure using this method from July 1, 2018 to June 30, 2022. The procedure involves controlled downsizing of the arterial sheath from 12 French (Fr) to 6 Fr catheters with intermittent compression to allow patent hemostasis facilitated by arterial recoil. Baseline characteristics and outcomes including closure success, immediate/delayed bleeding, and access site complications were included. Of 103 patients with Impella placement, 20 (19%) underwent LBA closure with this method. Patients were predominantly male (80%) and White (55%) with a mean age of 65 ± 16 years. After downsizing of the femoral sheath to 6 Fr, 14 patients underwent manual compression, 3 patients had a 6 Fr catheter left in place to maintain access, and 3 patients underwent placement of a Perclose or Vascade device. Successful LBA closure was performed in all patients with no immediate or delayed bleeding complications. Five patients (25%) died inpatient; the deaths were unrelated to complications of Impella removal. In conclusion, LBA closure post-Impella removal with this novel method was safe and effective. Further prospective studies are needed to ascertain its comparative efficacy.
MeSH term(s)	Humans ; Male ; Middle Aged ; Aged ; Aged, 80 and over ; Female ; Treatment Outcome ; Device Removal ; Percutaneous Coronary Intervention ; Femoral Artery/surgery ; Hemorrhage
Language	English
Publishing date	2023-11-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2079676-6
ISSN	1535-2811 ; 1535-282X
ISSN (online)	1535-2811
ISSN	1535-282X
DOI	10.1097/HPC.0000000000000343
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Zs.A 5660: Show issues

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Article ; Online: Deletion of PTEN in microglia ameliorates chronic neuroinflammation following repetitive mTBI.

Pearson, Andrew / Ortiz, Camila / Eisenbaum, Max / Arrate, Clara / Browning, Mackenzie / Mullan, Michael / Bachmeier, Corbin / Crawford, Fiona / Ojo, Joseph O

Molecular and cellular neurosciences

2023 Volume 125, Page(s) 103855

Abstract: Traumatic brain injury is a leading cause of morbidity and mortality in adults and children in developed nations. Following the primary injury, microglia, the resident innate immune cells of the CNS, initiate several inflammatory signaling cascades and ... ...

Abstract	Traumatic brain injury is a leading cause of morbidity and mortality in adults and children in developed nations. Following the primary injury, microglia, the resident innate immune cells of the CNS, initiate several inflammatory signaling cascades and pathophysiological responses that may persist chronically; chronic neuroinflammation following TBI has been closely linked to the development of neurodegeneration and neurological dysfunction. Phosphoinositide 3-kinases (PI3Ks) are a family of lipid kinases that have been shown to regulate several key mechanisms in the inflammatory response to TBI. Increasing evidence has shown that the modulation of the PI3K/AKT signaling pathway has the potential to influence the cellular response to inflammatory stimuli. However, directly targeting PI3K signaling poses several challenges due to its regulatory role in several cell survival pathways. We have previously identified that the phosphatase and tensin homolog deleted on chromosome 10 (PTEN), the major negative regulator of PI3K/AKT signaling, is dysregulated following exposure to repetitive mild traumatic brain injury (r-mTBI). Moreover, this dysregulated PI3K/AKT signaling was correlated with chronic microglial-mediated neuroinflammation. Therefore, we interrogated microglial-specific PTEN as a therapeutic target in TBI by generating a microglial-specific, Tamoxifen inducible conditional PTEN knockout model using a CX3CR1 Cre recombinase mouse line PTEN
MeSH term(s)	Animals ; Mice ; Brain Injuries, Traumatic/metabolism ; Disease Models, Animal ; Inflammation/metabolism ; Mice, Inbred C57BL ; Microglia/metabolism ; Neuroinflammatory Diseases ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Pten protein, mouse (EC 3.1.3.67)
Language	English
Publishing date	2023-04-20
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/j.mcn.2023.103855
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Zs.A 3035: Show issues

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Article: Age and

Huguenard, Claire J C / Cseresznye, Adam / Darcey, Teresa / Nkiliza, Aurore / Evans, James E / Hazen, Stanley L / Mullan, Michael / Crawford, Fiona / Abdullah, Laila

Frontiers in aging neuroscience

2023 Volume 14, Page(s) 1059017

Abstract: With age the apolipoprotein E ( ...

Abstract	With age the apolipoprotein E (
Language	English
Publishing date	2023-01-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2022.1059017
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