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Article ; Online: Effects of Sex and Western Diet on Spatial Lipidomic Profiles for the Hippocampus, Cortex, and Corpus Callosum in Mice Using MALDI MSI.

Shafer, Catelynn C / Di Lucente, Jacopo / Mendiola, Ulises Ruiz / Maezawa, Izumi / Jin, Lee-Way / Neumann, Elizabeth K

Journal of the American Society for Mass Spectrometry

2024

Abstract: Diet is inextricably linked to human health and biological functionality. Reduced cognitive function among other health issues has been correlated with a western diet (WD) in mouse models, indicating that increases in neurodegeneration could be fueled in ...

Abstract	Diet is inextricably linked to human health and biological functionality. Reduced cognitive function among other health issues has been correlated with a western diet (WD) in mouse models, indicating that increases in neurodegeneration could be fueled in part by a poor diet. In this study, we use matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI MSI) to spatially map the lipidomic profiles of male and female mice that were fed a high-fat, high-sucrose WD for a period of 7 weeks. Our findings concluded that the cortex and corpus callosum showed significant lipid variation by WD in female mice, while there was little to no variation in the hippocampus, regardless of sex. On the other hand, lipid profiles were significantly affected by sex in all regions. Overall, 83 lipids were putatively identified in the mouse brain; among them, HexCer(40:1;O3) and PE(34:0) were found to have the largest statistical difference based on diet for female mice in the cortex and corpus callosum, respectively. Additional lipid changes are noted and can serve as a metric for understanding the brain's metabolomic response to changes in diet, particularly as it relates to disease.
Language	English
Publishing date	2024-03-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	1073671-2
ISSN	1879-1123 ; 1044-0305
ISSN (online)	1879-1123
ISSN	1044-0305
DOI	10.1021/jasms.3c00446
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Article ; Online: H3G34-mutant diffuse hemispheric glioma with osseous metastases: a case report and literature review.

Yu, Nina / Lee, Han Sung / Raslan, Osama A / Jin, Lee-Way / Aboud, Orwa

CNS oncology

2023 Volume 12, Issue 2, Page(s) CNS95

Abstract: Aim: ...

Abstract	Aim:
MeSH term(s)	Female ; Humans ; Young Adult ; Adult ; Brain Neoplasms/diagnostic imaging ; Brain Neoplasms/genetics ; Brain Neoplasms/therapy ; Mutation ; Glioma/diagnostic imaging ; Glioma/genetics ; Glioma/pathology ; Central Nervous System Neoplasms
Language	English
Publishing date	2023-03-15
Publishing country	England
Document type	Review ; Case Reports ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2692808-5
ISSN	2045-0915 ; 2045-0915
ISSN (online)	2045-0915
ISSN	2045-0915
DOI	10.2217/cns-2022-0020
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Article: White matter injury, cholesterol dysmetabolism, and APP/Abeta dysmetabolism interact to produce Alzheimer's disease (AD) neuropathology: A hypothesis and review.

Sharp, Frank R / DeCarli, Charles S / Jin, Lee-Way / Zhan, Xinhua

Frontiers in aging neuroscience

2023 Volume 15, Page(s) 1096206

Abstract: We postulate that myelin injury contributes to cholesterol release from myelin and cholesterol dysmetabolism which contributes to Abeta dysmetabolism, and combined with genetic and AD risk factors, leads to increased Abeta and amyloid plaques. Increased ... ...

Abstract	We postulate that myelin injury contributes to cholesterol release from myelin and cholesterol dysmetabolism which contributes to Abeta dysmetabolism, and combined with genetic and AD risk factors, leads to increased Abeta and amyloid plaques. Increased Abeta damages myelin to form a vicious injury cycle. Thus, white matter injury, cholesterol dysmetabolism and Abeta dysmetabolism interact to produce or worsen AD neuropathology. The amyloid cascade is the leading hypothesis for the cause of Alzheimer's disease (AD). The failure of clinical trials based on this hypothesis has raised other possibilities. Even with a possible new success (Lecanemab), it is not clear whether this is a cause or a result of the disease. With the discovery in 1993 that the apolipoprotein E type 4 allele (APOE4) was the major risk factor for sporadic, late-onset AD (LOAD), there has been increasing interest in cholesterol in AD since APOE is a major cholesterol transporter. Recent studies show that cholesterol metabolism is intricately involved with Abeta (Aβ)/amyloid transport and metabolism, with cholesterol down-regulating the Aβ LRP1 transporter and upregulating the Aβ RAGE receptor, both of which would increase brain Aβ. Moreover, manipulating cholesterol transport and metabolism in rodent AD models can ameliorate pathology and cognitive deficits, or worsen them depending upon the manipulation. Though white matter (WM) injury has been noted in AD brain since Alzheimer's initial observations, recent studies have shown abnormal white matter in every AD brain. Moreover, there is age-related WM injury in normal individuals that occurs earlier and is worse with the APOE4 genotype. Moreover, WM injury precedes formation of plaques and tangles in human Familial Alzheimer's disease (FAD) and precedes plaque formation in rodent AD models. Restoring WM in rodent AD models improves cognition without affecting AD pathology. Thus, we postulate that the amyloid cascade, cholesterol dysmetabolism and white matter injury interact to produce and/or worsen AD pathology. We further postulate that the primary initiating event could be related to any of the three, with age a major factor for WM injury, diet and APOE4 and other genes a factor for cholesterol dysmetabolism, and FAD and other genes for Abeta dysmetabolism.
Language	English
Publishing date	2023-02-10
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2023.1096206
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Article: Lipopolysaccharide, Identified Using an Antibody and by PAS Staining, Is Associated With

Zhan, Xinhua / Hakoupian, Marisa / Jin, Lee-Way / Sharp, Frank R

Frontiers in aging neuroscience

2021 Volume 13, Page(s) 705594

Abstract: ... Corpora ... ...

Abstract	Corpora amylacea
Language	English
Publishing date	2021-11-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2021.705594
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Article ; Online: Preanalytic variable effects on segmentation and quantification machine learning algorithms for amyloid-β analyses on digitized human brain slides.

Oliveira, Luca Cerny / Lai, Zhengfeng / Harvey, Danielle / Nzenkue, Kevin / Jin, Lee-Way / Decarli, Charles / Chuah, Chen-Nee / Dugger, Brittany N

Journal of neuropathology and experimental neurology

2023 Volume 82, Issue 3, Page(s) 212–220

Abstract: Computational machine learning (ML)-based frameworks could be advantageous for scalable analyses in neuropathology. A recent deep learning (DL) framework has shown promise in automating the processes of visualizing and quantifying different types of ... ...

Abstract	Computational machine learning (ML)-based frameworks could be advantageous for scalable analyses in neuropathology. A recent deep learning (DL) framework has shown promise in automating the processes of visualizing and quantifying different types of amyloid-β deposits as well as segmenting white matter (WM) from gray matter (GM) on digitized immunohistochemically stained slides. However, this framework has only been trained and evaluated on amyloid-β-stained slides with minimal changes in preanalytic variables. In this study, we evaluated select preanalytical variables including magnification, compression rate, and storage format using three digital slides scanners (Zeiss Axioscan Z1, Leica Aperio AT2, and Leica Aperio GT 450), on over 60 whole slide images, in a cohort of 14 cases having a spectrum of amyloid-β deposits. We conducted statistical comparisons of preanalytic variables with repeated measures analysis of variance evaluating the outputs of two DL frameworks for segmentation and object classification tasks. For both WM/GM segmentation and amyloid-β plaque classification tasks, there were statistical differences with respect to scanner types (p < 0.05) and magnifications (p < 0.05). Although small numbers of cases were analyzed, this pilot study highlights the significance of preanalytic variables that may alter the performance of ML algorithms.
MeSH term(s)	Humans ; Algorithms ; Brain ; Image Processing, Computer-Assisted/methods ; Machine Learning ; Pilot Projects
Chemical Substances	APP protein, human
Language	English
Publishing date	2023-01-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/nlac132
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Ui II Zs.194: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

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Article ; Online: Vascular Risk Predicts Plasma Amyloid β 42/40 Through Cerebral Amyloid Burden in

Sapkota, Shraddha / Erickson, Kelsey / Fletcher, Evan / Tomaszewski Farias, Sarah E / Jin, Lee-Way / DeCarli, Charles

Stroke

2023 Volume 54, Issue 5, Page(s) 1227–1235

Abstract: Background: Understanding the neurobiological underpinnings between established multimodal dementia risk factors and noninvasive blood-based biomarkers may lead to greater precision and earlier identification of older adults at risk of accelerated ... ...

Abstract	Background: Understanding the neurobiological underpinnings between established multimodal dementia risk factors and noninvasive blood-based biomarkers may lead to greater precision and earlier identification of older adults at risk of accelerated decline and dementia. We examined whether key vascular and genetic risk impact the association between cerebral amyloid burden and plasma aβ (amyloid β) 42/40 in nondemented older adults. Methods: We used nondemented older adults from the UCD-ADRC (University of California, Davis-Alzheimer's Disease Research Center) study ( Results: Vascular risk significantly predicted cerebral amyloid burden in Alzheimer's Disease Neuroimaging Initiative but not in the UCD-ADRC cohort. Cerebral amyloid burden was associated with plasma aβ 42/40 in both cohorts. Higher vascular risk increased cerebral amyloid burden was indirectly associated with reduced plasma aβ 42/40 in Alzheimer's Disease Neuroimaging Initiative but not in UCD-ADRC cohort. However, when stratified by Conclusions: Vascular risk is indirectly associated with the level of plasma aβ 42/40 via cerebral amyloid burden only in
MeSH term(s)	Humans ; Aged ; Amyloid beta-Peptides/metabolism ; Alzheimer Disease/genetics ; Apolipoprotein E4/genetics ; Cross-Sectional Studies ; Brain/metabolism ; Positron-Emission Tomography ; Amyloid
Chemical Substances	amyloid beta-protein (1-42) ; Amyloid beta-Peptides ; Apolipoprotein E4 ; Amyloid
Language	English
Publishing date	2023-04-06
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	80381-9
ISSN	1524-4628 ; 0039-2499 ; 0749-7954
ISSN (online)	1524-4628
ISSN	0039-2499 ; 0749-7954
DOI	10.1161/STROKEAHA.122.041854
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Article: In vivo characterization of the human glioblastoma infiltrative edge with label-free intraoperative fluorescence lifetime imaging.

Alfonso-Garcia, Alba / Anbunesan, Silvia Noble / Bec, Julien / Lee, Han Sung / Jin, Lee-Way / Bloch, Orin / Marcu, Laura

Biomedical optics express

2023 Volume 14, Issue 5, Page(s) 2196–2208

Abstract: Challenges in identifying a glioblastoma's infiltrative edge during neurosurgical procedures result in rapid recurrence. A label-free fluorescence lifetime imaging (FLIm) device was used to evaluate glioblastoma's infiltrative ... ...

Abstract	Challenges in identifying a glioblastoma's infiltrative edge during neurosurgical procedures result in rapid recurrence. A label-free fluorescence lifetime imaging (FLIm) device was used to evaluate glioblastoma's infiltrative edge
Language	English
Publishing date	2023-04-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2572216-5
ISSN	2156-7085
ISSN	2156-7085
DOI	10.1364/BOE.481304
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Article ; Online: The role of FUT8-catalyzed core fucosylation in Alzheimer's amyloid-β oligomer-induced activation of human microglia.

Jin, Lee-Way / di Lucente, Jacopo / Ruiz Mendiola, Ulises / Tang, Xinyu / Zivkovic, Angela M / Lebrilla, Carlito B / Maezawa, Izumi

Glia

2023 Volume 71, Issue 5, Page(s) 1346–1359

Abstract: Fucosylation, especially core fucosylation of N-glycans catalyzed by α1-6 fucosyltransferase (fucosyltransferase 8 or FUT8), plays an important role in regulating the peripheral immune system and inflammation. However, its role in microglial activation ... ...

Abstract	Fucosylation, especially core fucosylation of N-glycans catalyzed by α1-6 fucosyltransferase (fucosyltransferase 8 or FUT8), plays an important role in regulating the peripheral immune system and inflammation. However, its role in microglial activation is poorly understood. Here we used human induced pluripotent stem cells-derived microglia (hiMG) as a model to study the role of FUT8-catalyzed core fucosylation in amyloid-β oligomer (AβO)-induced microglial activation, in view of its significant relevance to the pathogenesis of Alzheimer's disease (AD). HiMG responded to AβO and lipopolysaccharides (LPS) with a pattern of pro-inflammatory activation as well as enhanced core fucosylation and FUT8 expression within 24 h. Furthermore, we found increased FUT8 expression in both human AD brains and microglia isolated from 5xFAD mice, a model of AD-like cerebral amyloidosis. Inhibition of fucosylation in AβO-stimulated hiMG reduced the induction of pro-inflammatory cytokines, suppressed the activation of p38MAPK, and rectified phagocytic deficits. Specific inhibition of FUT8 by siRNA-mediated knockdown also reduced AβO-induced pro-inflammatory cytokines. We further showed that p53 binds to the two consensus binding sites in the Fut8 promoter, and that p53 knockdown abolished FUT8 overexpression in AβO-activated hiMG. Taken together, our evidence supports that FUT8-catalyzed core fucosylation is a signaling pathway required for AβO-induced microglia activation and that FUT8 is a component of the p53 signaling cascade regulating microglial behavior. Because microglia are a key driver of AD pathogenesis, our results suggest that microglial FUT8 could be an anti-inflammatory therapeutic target for AD.
MeSH term(s)	Humans ; Mice ; Animals ; Fucosyltransferases/metabolism ; Microglia/metabolism ; Amyloid beta-Peptides/metabolism ; Alzheimer Disease/metabolism ; Tumor Suppressor Protein p53 ; Induced Pluripotent Stem Cells/metabolism ; Cytokines/metabolism ; Catalysis
Chemical Substances	Fucosyltransferases (EC 2.4.1.-) ; Amyloid beta-Peptides ; Tumor Suppressor Protein p53 ; Cytokines
Language	English
Publishing date	2023-01-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24345
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Article: Aging, Plasminogen Activator Inhibitor 1, Brain Cell Senescence, and Alzheimer's Disease.

Jiang, Chun-Sun / Rana, Tapasi / Jin, Lee-Way / Farr, Susan A / Morley, John E / Qin, Hongwei / Liu, Gang / Liu, Rui-Ming

Aging and disease

2023 Volume 14, Issue 2, Page(s) 515–528

Abstract: The etiology for late-onset Alzheimer's disease (LOAD), which accounts for >95% of Alzheimer's disease (AD) cases, is unknown. Emerging evidence suggests that cellular senescence contributes importantly to AD pathophysiology, although the mechanisms ... ...

Abstract	The etiology for late-onset Alzheimer's disease (LOAD), which accounts for >95% of Alzheimer's disease (AD) cases, is unknown. Emerging evidence suggests that cellular senescence contributes importantly to AD pathophysiology, although the mechanisms underlying brain cell senescence and by which senescent cells promote neuro-pathophysiology remain unclear. In this study we show for the first time that the expression of plasminogen activator inhibitor 1 (PAI-1), a serine protease inhibitor, is increased, in correlation with the increased expression of cell cycle repressors p53 and p21, in the hippocampus/cortex of senescence accelerated mouse prone 8 (SAMP8) mice and LOAD patients. Double immunostaining results show that astrocytes in the brain of LOAD patients and SAMP8 mice express higher levels of senescent markers and PAI-1, compared to astrocytes in the corresponding controls. In vitro studies further show that overexpression of PAI-1 alone, intracellularly or extracellularly, induced senescence, whereas inhibition or silencing PAI-1 attenuated H
Language	English
Publishing date	2023-04-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2625789-0
ISSN	2152-5250
ISSN	2152-5250
DOI	10.14336/AD.2022.1220
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Article ; Online: Transcriptomic and glycomic analyses highlight pathway-specific glycosylation alterations unique to Alzheimer's disease.

Tang, Xinyu / Tena, Jennyfer / Di Lucente, Jacopo / Maezawa, Izumi / Harvey, Danielle J / Jin, Lee-Way / Lebrilla, Carlito B / Zivkovic, Angela M

Scientific reports

2023 Volume 13, Issue 1, Page(s) 7816

Abstract: Glycosylation has been found to be altered in the brains of individuals with Alzheimer's disease (AD). However, it is unknown which specific glycosylation-related pathways are altered in AD dementia. Using publicly available RNA-seq datasets covering ... ...

Abstract	Glycosylation has been found to be altered in the brains of individuals with Alzheimer's disease (AD). However, it is unknown which specific glycosylation-related pathways are altered in AD dementia. Using publicly available RNA-seq datasets covering seven brain regions and including 1724 samples, we identified glycosylation-related genes ubiquitously changed in individuals with AD. Several differentially expressed glycosyltransferases found by RNA-seq were confirmed by qPCR in a different set of human medial temporal cortex (MTC) samples (n = 20 AD vs. 20 controls). N-glycan-related changes predicted by expression changes in these glycosyltransferases were confirmed by mass spectrometry (MS)-based N-glycan analysis in the MTC (n = 9 AD vs. 6 controls). About 80% of glycosylation-related genes were differentially expressed in at least one brain region of AD participants (adjusted p-values < 0.05). Upregulation of MGAT1 and B4GALT1 involved in complex N-linked glycan formation and galactosylation, respectively, were reflected by increased concentrations of corresponding N-glycans. Isozyme-specific changes were observed in expression of the polypeptide N-acetylgalactosaminyltransferase (GALNT) family and the alpha-N-acetylgalactosaminide alpha-2,6-sialyltransferase (ST6GALNAC) family of enzymes. Several glycolipid-specific genes (UGT8, PIGM) were upregulated. The critical transcription factors regulating the expression of N-glycosylation and elongation genes were predicted and found to include STAT1 and HSF5. The miRNA predicted to be involved in regulating N-glycosylation and elongation glycosyltransferases were has-miR-1-3p and has-miR-16-5p, respectively. Our findings provide an overview of glycosylation pathways affected by AD and potential regulators of glycosyltransferase expression that deserve further validation and suggest that glycosylation changes occurring in the brains of AD dementia individuals are highly pathway-specific and unique to AD.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Glycosylation ; Transcriptome ; Glycomics ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Glycosyltransferases/genetics ; Glycosyltransferases/metabolism ; Polysaccharides/metabolism ; Mannosyltransferases/genetics
Chemical Substances	MicroRNAs ; Glycosyltransferases (EC 2.4.-) ; Polysaccharides ; PIGM protein, human (EC 2.4.1.-) ; Mannosyltransferases (EC 2.4.1.-)
Language	English
Publishing date	2023-05-15
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-34787-4
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