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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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Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

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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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bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: MMP9 modulation improves specific neurobehavioral deficits in a mouse model of Alzheimer's disease.

Ringland, Charis / Schweig, Jonas Elias / Eisenbaum, Maxwell / Paris, Daniel / Ait-Ghezala, Ghania / Mullan, Michael / Crawford, Fiona / Abdullah, Laila / Bachmeier, Corbin

BMC neuroscience

2021 Volume 22, Issue 1, Page(s) 39

Abstract: Background: Matrix metallopeptidase 9 (MMP9) has been implicated in a variety of neurological disorders, including Alzheimer's disease (AD), where MMP9 levels are elevated in the brain and cerebrovasculature. Previously our group demonstrated ... ...

Abstract	Background: Matrix metallopeptidase 9 (MMP9) has been implicated in a variety of neurological disorders, including Alzheimer's disease (AD), where MMP9 levels are elevated in the brain and cerebrovasculature. Previously our group demonstrated apolipoprotein E4 (apoE4) was less efficient in regulating MMP9 activity in the brain than other apoE isoforms, and that MMP9 inhibition facilitated beta-amyloid (Aβ) elimination across the blood-brain barrier (BBB) METHODS: In the current studies, we evaluated the impact of MMP9 modulation on Aβ disposition and neurobehavior in AD using two approaches, (1) pharmacological inhibition of MMP9 with SB-3CT in apoE4 x AD (E4FAD) mice, and (2) gene deletion of MMP9 in AD mice (MMP9KO/5xFAD) RESULTS: Treatment with the MMP9 inhibitor SB-3CT in E4FAD mice led to reduced anxiety compared to placebo using the elevated plus maze. Deletion of the MMP9 gene in 5xFAD mice also reduced anxiety using the open field test, in addition to improving sociability and social recognition memory, particularly in male mice, as assessed through the three-chamber task, indicating certain behavioral alterations in AD may be mediated by MMP9. However, neither pharmacological inhibition of MMP9 or gene deletion of MMP9 affected spatial learning or memory in the AD animals, as determined through the radial arm water maze. Moreover, the effect of MMP9 modulation on AD neurobehavior was not due to changes in Aβ disposition, as both brain and plasma Aβ levels were unchanged in the SB-3CT-treated E4FAD animals and MMP9KO/AD mice compared to their respective controls. Conclusions: In total, while MMP9 inhibition did improve specific neurobehavioral deficits associated with AD, such as anxiety and social recognition memory, modulation of MMP9 did not alter spatial learning and memory or Aβ tissue levels in AD animals. While targeting MMP9 may represent a therapeutic strategy to mitigate aspects of neurobehavioral decline in AD, further work is necessary to understand the nature of the relationship between MMP9 activity and neurological dysfunction.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Alzheimer Disease/psychology ; Amyloid beta-Peptides/genetics ; Animals ; Anxiety/drug therapy ; Anxiety/genetics ; Anxiety/metabolism ; Anxiety/psychology ; Brain/metabolism ; Female ; Heterocyclic Compounds, 1-Ring/pharmacology ; Heterocyclic Compounds, 1-Ring/therapeutic use ; Male ; Matrix Metalloproteinase 9/deficiency ; Matrix Metalloproteinase 9/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Activity/drug effects ; Motor Activity/physiology ; Presenilin-1/genetics ; Social Interaction/drug effects ; Spatial Learning/drug effects ; Spatial Learning/physiology ; Sulfones/pharmacology ; Sulfones/therapeutic use
Chemical Substances	Amyloid beta-Peptides ; Heterocyclic Compounds, 1-Ring ; Presenilin-1 ; SB 3CT compound ; Sulfones ; presenilin 1, mouse ; Matrix Metalloproteinase 9 (EC 3.4.24.35) ; Mmp9 protein, mouse (EC 3.4.24.35)
Language	English
Publishing date	2021-05-25
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2041344-0
ISSN	1471-2202 ; 1471-2202
ISSN (online)	1471-2202
ISSN	1471-2202
DOI	10.1186/s12868-021-00643-2
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Influence of traumatic brain injury on extracellular tau elimination at the blood-brain barrier.

Eisenbaum, Maxwell / Pearson, Andrew / Gratkowski, Arissa / Mouzon, Benoit / Mullan, Michael / Crawford, Fiona / Ojo, Joseph / Bachmeier, Corbin

Fluids and barriers of the CNS

2021 Volume 18, Issue 1, Page(s) 48

Abstract: Repetitive head trauma has been associated with the accumulation of tau species in the brain. Our prior work showed brain vascular mural cells contribute to tau processing in the brain, and that these cells progressively degenerate following repetitive ... ...

Abstract	Repetitive head trauma has been associated with the accumulation of tau species in the brain. Our prior work showed brain vascular mural cells contribute to tau processing in the brain, and that these cells progressively degenerate following repetitive mild traumatic brain injury (r-mTBI). The current studies investigated the role of the cerebrovasculature in the elimination of extracellular tau from the brain, and the influence of r-mTBI on these processes. Following intracranial injection of biotin-labeled tau, the levels of exogenous labeled tau residing in the brain were elevated in a mouse model of r-mTBI at 12 months post-injury compared to r-sham mice, indicating reduced tau elimination from the brain following head trauma. This may be the result of decreased caveolin-1 mediated tau efflux at the blood-brain barrier (BBB), as the caveolin inhibitor, methyl-β-cyclodextrin, significantly reduced tau uptake in isolated cerebrovessels and significantly decreased the basolateral-to-apical transit of tau across an in vitro model of the BBB. Moreover, we found that the upstream regulator of endothelial caveolin-1, Mfsd2a, was elevated in r-mTBI cerebrovessels compared to r-sham, which coincided with a decreased expression of cerebrovascular caveolin-1 in the chronic phase following r-mTBI (> 3 months post-injury). Lastly, angiopoietin-1, a mural cell-derived protein governing endothelial Mfsd2a expression, was secreted from r-mTBI cerebrovessels to a greater extent than r-sham animals. Altogether, in the chronic phase post-injury, release of angiopoietin-1 from degenerating mural cells downregulates caveolin-1 expression in brain endothelia, resulting in decreased tau elimination across the BBB, which may describe the accumulation of tau species in the brain following head trauma.
MeSH term(s)	Animals ; Blood-Brain Barrier/metabolism ; Brain Injuries, Traumatic/metabolism ; Disease Models, Animal ; Female ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; tau Proteins/metabolism
Chemical Substances	tau Proteins
Language	English
Publishing date	2021-10-26
Publishing country	England
Document type	Journal Article
ZDB-ID	2595406-4
ISSN	2045-8118 ; 2045-8118
ISSN (online)	2045-8118
ISSN	2045-8118
DOI	10.1186/s12987-021-00283-y
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Article ; Online: Apolipoprotein E isoforms differentially regulate matrix metallopeptidase 9 function in Alzheimer's disease.

Ringland, Charis / Schweig, Jonas Elias / Paris, Daniel / Shackleton, Ben / Lynch, Cillian E / Eisenbaum, Maxwell / Mullan, Michael / Crawford, Fiona / Abdullah, Laila / Bachmeier, Corbin

Neurobiology of aging

2020 Volume 95, Page(s) 56–68

Abstract: Apolipoprotein E (APOE) has been shown to influence amyloid-β (Aβ) clearance from the brain in an isoform-specific manner. Our prior work showed that Aβ transit across the blood-brain-barrier was reduced by apoE4, compared to other apoE isoforms, due to ... ...

Abstract	Apolipoprotein E (APOE) has been shown to influence amyloid-β (Aβ) clearance from the brain in an isoform-specific manner. Our prior work showed that Aβ transit across the blood-brain-barrier was reduced by apoE4, compared to other apoE isoforms, due to elevated lipoprotein receptor shedding in brain endothelia. Recently, we demonstrated that matrix metallopeptidase 9 (MMP-9) induces lipoprotein receptor proteolysis in an apoE isoform-dependent manner, which impacts Aβ elimination from the brain. The current studies interrogated the relationship between apoE and MMP-9 and found that apoE impacted proMMP-9 cellular secretion from brain endothelia (apoE2 < apoE3 = apoE4). In a cell-free assay, apoE dose-dependently reduced MMP-9 activity, with apoE4 showing a significantly weaker ability to inhibit MMP-9 function than apoE2 or apoE3. Finally, we observed elevated MMP-9 expression and activity in the cerebrovasculature of both human and animal AD brain specimens with an APOE4 genotype. Collectively, these findings suggest a role for apoE in regulating MMP-9 disposition and may describe the effect of apoE4 on Aβ pathology in the AD brain.
MeSH term(s)	Alzheimer Disease/etiology ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Animals ; Apolipoproteins E/genetics ; Apolipoproteins E/pharmacology ; Apolipoproteins E/physiology ; Brain/metabolism ; Dose-Response Relationship, Drug ; Endothelium/metabolism ; Genotype ; Humans ; Matrix Metalloproteinase 9/metabolism ; Matrix Metalloproteinase 9/physiology ; Matrix Metalloproteinase Inhibitors ; Protein Isoforms/physiology ; Proteolysis ; Receptors, Lipoprotein/metabolism
Chemical Substances	Amyloid beta-Peptides ; Apolipoproteins E ; Matrix Metalloproteinase Inhibitors ; Protein Isoforms ; Receptors, Lipoprotein ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2020-07-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	604505-4
ISSN	1558-1497 ; 0197-4580
ISSN (online)	1558-1497
ISSN	0197-4580
DOI	10.1016/j.neurobiolaging.2020.06.018
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Zs.A 1685: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 10: Show issues

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Article ; Online: Impairment of cerebrovascular reactivity in response to hypercapnic challenge in a mouse model of repetitive mild traumatic brain injury.

Lynch, Cillian E / Eisenbaum, Maxwell / Algamal, Moustafa / Balbi, Matilde / Ferguson, Scott / Mouzon, Benoit / Saltiel, Nicole / Ojo, Joseph / Diaz-Arrastia, Ramon / Mullan, Mike / Crawford, Fiona / Bachmeier, Corbin

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

2020 Volume 41, Issue 6, Page(s) 1362–1378

Abstract: Incidences of repetitive mild TBI (r-mTBI), like those sustained by contact sports athletes and military personnel, are thought to be a risk factor for development of neurodegenerative disorders. Those suffering from chronic TBI-related illness ... ...

Abstract	Incidences of repetitive mild TBI (r-mTBI), like those sustained by contact sports athletes and military personnel, are thought to be a risk factor for development of neurodegenerative disorders. Those suffering from chronic TBI-related illness demonstrate deficits in cerebrovascular reactivity (CVR), the ability of the cerebral vasculature to respond to a vasoactive stimulus. CVR is thus an important measure of traumatic cerebral vascular injury (TCVI), and a possible in vivo endophenotype of TBI-related neuropathogenesis. We combined laser speckle imaging of CVR in response to hypercapnic challenge with neurobehavioral assessment of learning and memory, to investigate if decreased cerebrovascular responsiveness underlies impaired cognitive function in our mouse model of chronic r-mTBI. We demonstrate a profile of blunted hypercapnia-evoked CVR in the cortices of r-mTBI mice like that of human TBI, alongside sustained memory and learning impairment, without biochemical or immunohistopathological signs of cerebral vessel laminar or endothelium constituent loss. Transient decreased expression of alpha smooth muscle actin and platelet-derived growth factor receptor β, indicative of TCVI, is obvious only at the time of the most pronounced CVR deficit. These findings implicate CVR as a valid preclinical measure of TCVI, perhaps useful for developing therapies targeting TCVI after recurrent mild head trauma.
MeSH term(s)	Animals ; Brain Concussion/physiopathology ; Cerebrovascular Circulation/physiology ; Disease Models, Animal ; Hypercapnia/complications ; Hypercapnia/physiopathology ; Male ; Mice ; Mice, Inbred C57BL
Language	English
Publishing date	2020-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	604628-9
ISSN	1559-7016 ; 0271-678X
ISSN (online)	1559-7016
ISSN	0271-678X
DOI	10.1177/0271678X20954015
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Zs.A 1663: Show issues

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Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Sensitive Detection of Exosomal Proteins via a Compact Surface Plasmon Resonance Biosensor for Cancer Diagnosis.

Liu, Chang / Zeng, Xie / An, Zijian / Yang, Yunchen / Eisenbaum, Maxwell / Gu, Xiaodong / Jornet, Josep M / Dy, Grace K / Reid, Mary E / Gan, Qiaoqiang / Wu, Yun

ACS sensors

2018 Volume 3, Issue 8, Page(s) 1471–1479

Abstract: Exosomes are small extracellular vesicles released by cells for cell-cell communication. They play important roles in cancer development, metastasis, and drug resistance. Exosomal proteins have been demonstrated by many studies as promising biomarkers ... ...

Abstract	Exosomes are small extracellular vesicles released by cells for cell-cell communication. They play important roles in cancer development, metastasis, and drug resistance. Exosomal proteins have been demonstrated by many studies as promising biomarkers for cancer screening, diagnosis, and monitoring. Among many detection techniques, surface plasmon resonance (SPR) is a highly sensitive, label-free, and real-time optical detection method. Commercial prism-based wavelength/angular-modulated SPR sensors afford high sensitivity and resolution, but their large footprint and high cost limit their adaptability for clinical settings. Recently, a nanoplasmonic exosome (nPLEX) assay was developed to detect exosomal proteins for ovarian cancer diagnosis. However, comparing with conventional SPR biosensors, the broad applications of nanoplasmonic biosensors are limited by the difficult and expensive fabrication of nanostructures. We have developed an intensity-modulated, compact SPR biosensor (25 cm × 10 cm × 25 cm) which uses a conventional SPR sensing mechanism and does not require nanostructure fabrication. Calibration from glycerol showed that the compact SPR biosensor offered sensitivity of 9.258 × 10
MeSH term(s)	Aged ; B7-H1 Antigen/analysis ; Biomarkers, Tumor/analysis ; Biosensing Techniques/methods ; Carcinoma, Non-Small-Cell Lung/diagnosis ; Cell Line, Tumor ; ErbB Receptors/analysis ; Exosomes/metabolism ; Female ; Humans ; Lung Neoplasms/diagnosis ; Male ; Middle Aged ; Protein Array Analysis ; Surface Plasmon Resonance ; Surface Properties
Chemical Substances	B7-H1 Antigen ; Biomarkers, Tumor ; CD274 protein, human ; ErbB Receptors (EC 2.7.10.1)
Language	English
Publishing date	2018-07-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	2379-3694
ISSN (online)	2379-3694
DOI	10.1021/acssensors.8b00230
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Article ; Online: ApoE4 expression disrupts tau uptake, trafficking, and clearance in astrocytes.

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

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Article ; Online: MMP9 modulation improves specific neurobehavioral deficits in a mouse model of Alzheimer's disease.

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Article ; Online: Influence of traumatic brain injury on extracellular tau elimination at the blood-brain barrier.

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Article ; Online: Apolipoprotein E isoforms differentially regulate matrix metallopeptidase 9 function in Alzheimer's disease.

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Article ; Online: Impairment of cerebrovascular reactivity in response to hypercapnic challenge in a mouse model of repetitive mild traumatic brain injury.

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Article ; Online: Sensitive Detection of Exosomal Proteins via a Compact Surface Plasmon Resonance Biosensor for Cancer Diagnosis.

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