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Article ; Online: Vascular Heparan Sulfate and Amyloid-β in Alzheimer's Disease Patients.

McMillan, Ilayda Ozsan / Gearing, Marla / Wang, Lianchun

International journal of molecular sciences

2024 Volume 25, Issue 7

Abstract: Alzheimer's disease (AD) is a debilitating neurodegenerative disease characterized by the accumulation of extracellular amyloid-β peptides (Aβ) within the cerebral parenchyma and vasculature, which is known as cerebral amyloid angiopathy (CAA). This ... ...

Abstract	Alzheimer's disease (AD) is a debilitating neurodegenerative disease characterized by the accumulation of extracellular amyloid-β peptides (Aβ) within the cerebral parenchyma and vasculature, which is known as cerebral amyloid angiopathy (CAA). This study utilized confocal imaging to investigate heparan sulfate (HS) expression within the cerebrovasculature and its associations with Aβ, gender, and ApoE4 genotype in AD. Our investigation revealed elevated levels of HS in the cerebrovasculature of AD patients with severe CAA. Additionally, these patients exhibited higher HS colocalization with Aβ in the cerebrovasculature, including both endothelial and vascular smooth muscle cell compartments. Intriguingly, a reversal in the polarized expression of HS within the cerebrovasculature was detected in AD patients with severe CAA. Furthermore, male patients exhibited lower levels of both parenchymal and cerebrovascular HS. Additionally, ApoE4 carriers displayed heightened cerebrovascular Aβ expression and a tendency of elevated cerebrovascular HS levels in AD patients with severe CAA. Overall, these findings reveal potential intricate interplay between HS, Aβ, ApoE, and vascular pathology in AD, thereby underscoring the potential roles of cerebrovascular HS in CAA development and AD pathology. Further study of the underlying mechanisms may present novel therapeutic avenues for AD treatment.
MeSH term(s)	Humans ; Male ; Alzheimer Disease/genetics ; Neurodegenerative Diseases ; Apolipoprotein E4/genetics ; Amyloid beta-Peptides ; Cerebral Amyloid Angiopathy ; Heparitin Sulfate
Chemical Substances	Apolipoprotein E4 ; Amyloid beta-Peptides ; Heparitin Sulfate (9050-30-0)
Language	English
Publishing date	2024-04-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25073964
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Article ; Online: Suppression of luteinizing hormone release by the α

Gearing, Marla / Terasawa, Ei

American journal of primatology

2020 Volume 25, Issue 1, Page(s) 23–33

Abstract: The effects of adrenergic antagonists on LH release were examined in ovariectomized female rhesus monkeys implanted with indwelling jugular catheters. While the ... ...

Abstract	The effects of adrenergic antagonists on LH release were examined in ovariectomized female rhesus monkeys implanted with indwelling jugular catheters. While the α
Language	English
Publishing date	2020-01-15
Publishing country	United States
Document type	Journal Article
ZDB-ID	1495834-X
ISSN	1098-2345 ; 0275-2565
ISSN (online)	1098-2345
ISSN	0275-2565
DOI	10.1002/ajp.1350250103
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Article: Histological Confirmation of Myelinated Neural Filaments Within the Tip of the Neurotrophic Electrode After a Decade of Neural Recordings.

Gearing, Marla / Kennedy, Philip

Frontiers in human neuroscience

2020 Volume 14, Page(s) 111

Abstract: Aim: Electrodes that provide brain to machine or computer interfacing must survive the lifetime of the person to be considered an acceptable prosthetic. The electrodes may be external such as with electroencephalographic (EEG), internal extracortical ... ...

Abstract	Aim: Electrodes that provide brain to machine or computer interfacing must survive the lifetime of the person to be considered an acceptable prosthetic. The electrodes may be external such as with electroencephalographic (EEG), internal extracortical such as electrocorticographic (ECoG) or intracortical. Methods: Most intracortical electrodes are placed close to the neuropil being recorded and do not survive years of recording. However, the Neurotrophic Electrode is placed within the cortex and the neuropil grows inside and through the hollow tip of the electrode and is thus trapped inside. Highly flexible coiled lead wires minimize the strain on the electrode tip. Histological analysis includes immunohistochemical detection of neurofilaments and the absence of gliosis. Results: This configuration led to a decade long recording in this locked-in person. At year nine, the neural activity underwent conditioning experiments indicating that the neural activity was functional and not noise. This paper presents data on the histological analysis of the tissue inside the electrode tip after 13 years of implantation. Conclusion: This paper is a singular example of histological analysis after a decade of recording. The histological analysis laid out herein is strong evidence that the brain can grow neurites into the electrode tip and record for a decade. This is profoundly important in the field of brain to machine or computer interfacing by implying that long term electrodes should incorporate some means of growing the neuropil into the electrode rather than placing the electrode into the neuropil.
Language	English
Publishing date	2020-04-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2425477-0
ISSN	1662-5161
ISSN	1662-5161
DOI	10.3389/fnhum.2020.00111
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Article ; Online: Tau deposition in the spinal cord is not specific for CTE-ALS.

Fournier, Christina N / Gearing, Marla / Glass, Jonathan D

Neurology

2020 Volume 95, Issue 1, Page(s) 37–39

MeSH term(s)	Amyotrophic Lateral Sclerosis/complications ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Chronic Traumatic Encephalopathy/complications ; Chronic Traumatic Encephalopathy/metabolism ; Chronic Traumatic Encephalopathy/pathology ; Female ; Humans ; Male ; Middle Aged ; Spinal Cord/metabolism ; Spinal Cord/pathology ; tau Proteins/analysis ; tau Proteins/metabolism
Chemical Substances	MAPT protein, human ; tau Proteins
Language	English
Publishing date	2020-06-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000009729
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Article ; Online: MicroRNA-650 Regulates the Pathogenesis of Alzheimer's Disease Through Targeting Cyclin-Dependent Kinase 5.

Lin, Li / Liu, Xiaodong / Cheng, Xuejun / Li, Yujing / Gearing, Marla / Levey, Allan / Huang, Xiaoli / Li, Ying / Jin, Peng / Li, Xuekun

Molecular neurobiology

2023 Volume 60, Issue 5, Page(s) 2426–2441

Abstract: Alzheimer's disease (AD) pathogenesis feature progressive neurodegeneration, amyloid-β plaque formation, and neurofibrillary tangles. Ample evidence has indicated the involvement of epigenetic pathways in AD pathogenesis. Here, we show that the ... ...

Abstract	Alzheimer's disease (AD) pathogenesis feature progressive neurodegeneration, amyloid-β plaque formation, and neurofibrillary tangles. Ample evidence has indicated the involvement of epigenetic pathways in AD pathogenesis. Here, we show that the expression of microRNA 650 (miR-650) is altered in brains from AD patients. Furthermore, we found that the processing of primary miR-650 to mature miR-650 is misregulated. Bioinformatic analysis predicted that miR-650 targets the expression of three AD-associated components: Apolipoprotein E (APOE), Presenilin 1 (PSEN1), and Cyclin-Dependent Kinase 5 (CDK5), and we have experimentally confirmed that miR-650 is able to significantly reduce the expression of APOE, PSEN1, and CDK5 in vitro. Importantly, the overexpression of miR-650 was further shown to significantly alter the CDK5 level and ameliorate AD pathologies in APP-PSEN1 transgenic mice. Overall, our results indicate that miR-650 influences AD pathogenesis through regulation of CDK5.
MeSH term(s)	Mice ; Animals ; Alzheimer Disease/pathology ; Cyclin-Dependent Kinase 5/genetics ; Cyclin-Dependent Kinase 5/metabolism ; Neurofibrillary Tangles/metabolism ; Mice, Transgenic ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Apolipoproteins E/metabolism ; Amyloid beta-Protein Precursor/metabolism ; Amyloid beta-Peptides/metabolism
Chemical Substances	Cyclin-Dependent Kinase 5 (EC 2.7.11.1) ; MicroRNAs ; Apolipoproteins E ; Amyloid beta-Protein Precursor ; Amyloid beta-Peptides
Language	English
Publishing date	2023-01-19
Publishing country	United States
Document type	Journal Article
ZDB-ID	645020-9
ISSN	1559-1182 ; 0893-7648
ISSN (online)	1559-1182
ISSN	0893-7648
DOI	10.1007/s12035-023-03224-y
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Article ; Online: Association of PM

Christensen, Grace M / Li, Zhenjiang / Liang, Donghai / Ebelt, Stefanie / Gearing, Marla / Levey, Allan I / Lah, James J / Wingo, Aliza / Wingo, Thomas / Hüls, Anke

Neurology

2024 Volume 102, Issue 5, Page(s) e209162

Abstract: Background and objectives: Fine particulate matter (PM: Methods: A cross-sectional study was conducted using brain tissue donors enrolled in the Emory Goizueta AD Research Center who died before 2020 (n = 224). Donors were assessed for AD pathology ... ...

Abstract	Background and objectives: Fine particulate matter (PM Methods: A cross-sectional study was conducted using brain tissue donors enrolled in the Emory Goizueta AD Research Center who died before 2020 (n = 224). Donors were assessed for AD pathology including the Braak stage, Consortium to Establish a Registry for AD (CERAD) score, and combined AD neuropathologic change (ABC) score. Traffic-related PM Results: Among the 224 participants, the mean age of death was 76 years, and 57% had at least 1 Discussion: Our study found traffic-related PM
MeSH term(s)	Humans ; Aged ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Apolipoprotein E4/genetics ; Cross-Sectional Studies ; Genotype ; Brain/pathology ; Apolipoproteins E/genetics
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E
Language	English
Publishing date	2024-02-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000209162
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Article ; Online: Differential DNA methylation in the brain as potential mediator of the association between traffic-related PM

Li, Zhenjiang / Liang, Donghai / Ebelt, Stefanie / Gearing, Marla / Kobor, Michael S / Konwar, Chaini / Maclsaac, Julie L / Dever, Kristy / Wingo, Aliza P / Levey, Allan I / Lah, James J / Wingo, Thomas S / Hüls, Anke

Alzheimer's & dementia : the journal of the Alzheimer's Association

2024 Volume 20, Issue 4, Page(s) 2538–2551

Abstract: Introduction: Growing evidence indicates that fine particulate matter (PM: Methods: We assessed genome-wide DNAm (Illumina EPIC BeadChips) in prefrontal cortex tissue and three AD-related neuropathological markers (Braak stage, CERAD, ABC score) for ... ...

Abstract	Introduction: Growing evidence indicates that fine particulate matter (PM Methods: We assessed genome-wide DNAm (Illumina EPIC BeadChips) in prefrontal cortex tissue and three AD-related neuropathological markers (Braak stage, CERAD, ABC score) for 159 donors, and estimated donors' residential traffic-related PM Results: PM Discussion: Our findings suggest differential DNAm related to neuroinflammation mediates the association between traffic-related PM Highlights: First study to evaluate the potential mediation effect of DNA methylation for the association between PM2.5 exposure and neuropathological changes of Alzheimer's disease. Study was based on brain tissues rarely investigated in previous air pollution research. Cg10495669, assigned to RBCK1 gene playing a role in inflammation, was associated consistently with 1-year, 3-year, and 5-year traffic-related PM2.5 exposures prior to death. Meet-in-the-middle approach and high-dimensional mediation analysis were used simultaneously to increase the potential of identifying the differentially methylated CpGs. Differential DNAm related to neuroinflammation was found to mediate the association between traffic-related PM2.5 and Alzheimer's disease.
MeSH term(s)	Humans ; DNA Methylation ; Alzheimer Disease/genetics ; Neuroinflammatory Diseases ; Particulate Matter/adverse effects ; Brain
Chemical Substances	Particulate Matter
Language	English
Publishing date	2024-02-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13650
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Article ; Online: An early proinflammatory transcriptional response to tau pathology is age-specific and foreshadows reduced tau burden.

Rasmussen, Jay / Ewing, Adam D / Bodea, Liviu-Gabriel / Bodea, Gabriela O / Gearing, Marla / Faulkner, Geoffrey J

Brain pathology (Zurich, Switzerland)

2021 Volume 32, Issue 3, Page(s) e13018

Abstract: Age is one of the strongest risk factors for the development of neurodegenerative diseases, the majority of which involve misfolded protein aggregates in the brain. These protein aggregates are thought to drive pathology and are attractive targets for ... ...

Abstract	Age is one of the strongest risk factors for the development of neurodegenerative diseases, the majority of which involve misfolded protein aggregates in the brain. These protein aggregates are thought to drive pathology and are attractive targets for the development of new therapies. However, it is unclear how age influences the onset of pathology and the accompanying molecular response. To address this knowledge gap, we used a model of seeded tau pathology to profile the transcriptomic changes in 3 and 12 month old mice in response to developing tau hyperphosphorylation and aggregation. First, we found the burden of hyperphosphorylated tau pathology in mice injected at 12 months of age was moderately reduced compared to animals injected at 3 months. On a molecular level, we found an inflammation-related subset of genes, including C3 and the disease-associated microglia genes Ctsd, Cst7, and Clec7a, were more expressed early in disease in 12 but not 3 month old mice. These findings provide evidence of an early, age-specific response to tau pathology, which could serve as a marker for the severity of downstream pathology.
MeSH term(s)	Age Factors ; Alzheimer Disease/pathology ; Animals ; Disease Models, Animal ; Mice ; Mice, Transgenic ; Microglia/pathology ; Protein Aggregates ; tau Proteins/genetics ; tau Proteins/metabolism
Chemical Substances	Protein Aggregates ; tau Proteins
Language	English
Publishing date	2021-08-31
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.13018
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Article ; Online: Reader response: Pathologic Thr

Glass, Jonathan D / Fournier, Christina N / Gearing, Marla

Neurology

2018 Volume 91, Issue 12, Page(s) 578–579

MeSH term(s)	Amyotrophic Lateral Sclerosis ; Humans ; Phosphorylation ; tau Proteins
Chemical Substances	tau Proteins
Language	English
Publishing date	2018-09-17
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000006192
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Article ; Online: The association between neighborhood deprivation and DNA methylation in an autopsy cohort.

Pett, Lindsay / Li, Zhenjiang / Abrishamcar, Sarina / Hodge, Kenyaita / Everson, Todd / Christensen, Grace / Gearing, Marla / Kobor, Michael S / Konwar, Chaini / MacIsaac, Julia L / Dever, Kristy / Wingo, Aliza P / Levey, Allan / Lah, James J / Wingo, Thomas S / Hüls, Anke

Aging

2024 Volume 16

Abstract: Previous research has found that living in a disadvantaged neighborhood is associated with poor health outcomes. Living in disadvantaged neighborhoods may alter inflammation and immune response in the body, which could be reflected in epigenetic ... ...

Abstract	Previous research has found that living in a disadvantaged neighborhood is associated with poor health outcomes. Living in disadvantaged neighborhoods may alter inflammation and immune response in the body, which could be reflected in epigenetic mechanisms such as DNA methylation (DNAm). We used robust linear regression models to conduct an epigenome-wide association study examining the association between neighborhood deprivation (Area Deprivation Index; ADI), and DNAm in brain tissue from 159 donors enrolled in the Emory Goizueta Alzheimer's Disease Research Center (Georgia, USA). We found one CpG site (cg26514961, gene
Language	English
Publishing date	2024-04-24
Publishing country	United States
Document type	Journal Article
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.205764
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