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Article: Comparative brain metabolomics reveals shared and distinct metabolic alterations in Alzheimer's disease and progressive supranuclear palsy.

Batra, Richa / Krumsiek, Jan / Wang, Xue / Allen, Mariet / Blach, Colette / Kastenmüller, Gabi / Arnold, Matthias / Ertekin-Taner, Nilüfer / Kaddurah-Daouk, Rima F

medRxiv : the preprint server for health sciences

2023

Abstract: Metabolic dysregulation is a hallmark of neurodegenerative diseases, including Alzheimer's disease (AD) and progressive supranuclear palsy (PSP). While metabolic dysregulation is a common link between these two tauopathies, a comprehensive brain ... ...

Abstract	Metabolic dysregulation is a hallmark of neurodegenerative diseases, including Alzheimer's disease (AD) and progressive supranuclear palsy (PSP). While metabolic dysregulation is a common link between these two tauopathies, a comprehensive brain metabolic comparison of the diseases has not yet been performed. We analyzed 342 postmortem brain samples from the Mayo Clinic Brain Bank and examined 658 metabolites in the cerebellar cortex and the temporal cortex between the two tauopathies. Our findings indicate that both diseases display oxidative stress associated with lipid metabolism, mitochondrial dysfunction linked to lysine metabolism, and an indication of tau-induced polyamine stress response. However, specific to AD, we detected glutathione-related neuroinflammation, deregulations of enzymes tied to purines, and cognitive deficits associated with vitamin B. Taken together, our findings underscore vast alterations in the brain's metabolome, illuminating shared neurodegenerative pathways and disease-specific traits in AD and PSP.
Language	English
Publishing date	2023-07-27
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.07.25.23293055
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Article ; Online: Titration-based normalization of antibody amount improves consistency of ChIP-seq experiments.

Caride, Ariel / Jang, Jin Sung / Shi, Geng-Xian / Lenz, Sam / Zhong, Jian / Kim, Kwan Hyun / Allen, Mariet / Robertson, Keith D / Farrugia, Gianrico / Ordog, Tamas / Ertekin-Taner, Nilüfer / Lee, Jeong-Heon

BMC genomics

2023 Volume 24, Issue 1, Page(s) 171

Abstract: Chromatin immunoprecipitation (ChIP) is an antibody-based approach that is frequently utilized in chromatin biology and epigenetics. The challenge in experimental variability by unpredictable nature of usable input amounts from samples and undefined ... ...

Abstract	Chromatin immunoprecipitation (ChIP) is an antibody-based approach that is frequently utilized in chromatin biology and epigenetics. The challenge in experimental variability by unpredictable nature of usable input amounts from samples and undefined antibody titer in ChIP reaction still remains to be addressed. Here, we introduce a simple and quick method to quantify chromatin inputs and demonstrate its utility for normalizing antibody amounts to the optimal titer in individual ChIP reactions. For a proof of concept, we utilized ChIP-seq validated antibodies against the key enhancer mark, acetylation of histone H3 on lysine 27 (H3K27ac), in the experiments. The results indicate that the titration-based normalization of antibody amounts improves assay outcomes including the consistency among samples both within and across experiments for a broad range of input amounts.
MeSH term(s)	Chromatin Immunoprecipitation Sequencing/methods ; Chromatin Immunoprecipitation/methods ; Histones/genetics ; Chromatin ; Antibodies
Chemical Substances	Histones ; Chromatin ; Antibodies
Language	English
Publishing date	2023-04-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2041499-7
ISSN	1471-2164 ; 1471-2164
ISSN (online)	1471-2164
ISSN	1471-2164
DOI	10.1186/s12864-023-09253-0
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Article ; Online: The landscape of metabolic brain alterations in Alzheimer's disease.

Batra, Richa / Arnold, Matthias / Wörheide, Maria A / Allen, Mariet / Wang, Xue / Blach, Colette / Levey, Allan I / Seyfried, Nicholas T / Ertekin-Taner, Nilüfer / Bennett, David A / Kastenmüller, Gabi / Kaddurah-Daouk, Rima F / Krumsiek, Jan

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

2022

Abstract: Introduction: Alzheimer's disease (AD) is accompanied by metabolic alterations both in the periphery and the central nervous system. However, so far, a global view of AD-associated metabolic changes in the brain has been missing.: Methods: We ... ...

Abstract	Introduction: Alzheimer's disease (AD) is accompanied by metabolic alterations both in the periphery and the central nervous system. However, so far, a global view of AD-associated metabolic changes in the brain has been missing. Methods: We metabolically profiled 500 samples from the dorsolateral prefrontal cortex. Metabolite levels were correlated with eight clinical parameters, covering both late-life cognitive performance and AD neuropathology measures. Results: We observed widespread metabolic dysregulation associated with AD, spanning 298 metabolites from various AD-relevant pathways. These included alterations to bioenergetics, cholesterol metabolism, neuroinflammation, and metabolic consequences of neurotransmitter ratio imbalances. Our findings further suggest impaired osmoregulation as a potential pathomechanism in AD. Finally, inspecting the interplay of proteinopathies provided evidence that metabolic associations were largely driven by tau pathology rather than amyloid beta pathology. Discussion: This work provides a comprehensive reference map of metabolic brain changes in AD that lays the foundation for future mechanistic follow-up studies.
Language	English
Publishing date	2022-07-13
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.12714
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Article ; Online: Nerve growth factor receptor (Ngfr) induces neurogenic plasticity by suppressing reactive astroglial Lcn2/Slc22a17 signaling in Alzheimer's disease.

NPJ Regenerative medicine

2023 Volume 8, Issue 1, Page(s) 33

Abstract: Neurogenesis, crucial for brain resilience, is reduced in Alzheimer's disease (AD) that induces astroglial reactivity at the expense of the pro-neurogenic potential, and restoring neurogenesis could counteract neurodegenerative pathology. However, the ... ...

Abstract	Neurogenesis, crucial for brain resilience, is reduced in Alzheimer's disease (AD) that induces astroglial reactivity at the expense of the pro-neurogenic potential, and restoring neurogenesis could counteract neurodegenerative pathology. However, the molecular mechanisms promoting pro-neurogenic astroglial fate despite AD pathology are unknown. In this study, we used APP/PS1dE9 mouse model and induced Nerve growth factor receptor (Ngfr) expression in the hippocampus. Ngfr, which promotes neurogenic fate of astroglia during the amyloid pathology-induced neuroregeneration in zebrafish brain, stimulated proliferative and neurogenic outcomes. Histological analyses of the changes in proliferation and neurogenesis, single-cell transcriptomics, spatial proteomics, and functional knockdown studies showed that the induced expression of Ngfr reduced the reactive astrocyte marker Lipocalin-2 (Lcn2), which we found was sufficient to reduce neurogenesis in astroglia. Anti-neurogenic effects of Lcn2 was mediated by Slc22a17, blockage of which recapitulated the pro-neurogenicity by Ngfr. Long-term Ngfr expression reduced amyloid plaques and Tau phosphorylation. Postmortem human AD hippocampi and 3D human astroglial cultures showed elevated LCN2 levels correlate with reactive gliosis and reduced neurogenesis. Comparing transcriptional changes in mouse, zebrafish, and human AD brains for cell intrinsic differential gene expression and weighted gene co-expression networks revealed common altered downstream effectors of NGFR signaling, such as PFKP, which can enhance proliferation and neurogenesis in vitro when blocked. Our study suggests that the reactive non-neurogenic astroglia in AD can be coaxed to a pro-neurogenic fate and AD pathology can be alleviated with Ngfr. We suggest that enhancing pro-neurogenic astroglial fate may have therapeutic ramifications in AD.
Language	English
Publishing date	2023-07-10
Publishing country	United States
Document type	Journal Article
ISSN	2057-3995
ISSN (online)	2057-3995
DOI	10.1038/s41536-023-00311-5
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Article ; Online: Cross species systems biology discovers glial DDR2, STOM, and KANK2 as therapeutic targets in progressive supranuclear palsy.

Nature communications

2023 Volume 14, Issue 1, Page(s) 6801

Abstract: Progressive supranuclear palsy (PSP) is a neurodegenerative parkinsonian disorder characterized by cell-type-specific tau lesions in neurons and glia. Prior work uncovered transcriptome changes in human PSP brains, although their cell-specificity is ... ...

Abstract	Progressive supranuclear palsy (PSP) is a neurodegenerative parkinsonian disorder characterized by cell-type-specific tau lesions in neurons and glia. Prior work uncovered transcriptome changes in human PSP brains, although their cell-specificity is unknown. Further, systematic data integration and experimental validation platforms to prioritize brain transcriptional perturbations as therapeutic targets in PSP are currently lacking. In this study, we combine bulk tissue (n = 408) and single nucleus RNAseq (n = 34) data from PSP and control brains with transcriptome data from a mouse tauopathy and experimental validations in Drosophila tau models for systematic discovery of high-confidence expression changes in PSP with therapeutic potential. We discover, replicate, and annotate thousands of differentially expressed genes in PSP, many of which reside in glia-enriched co-expression modules and cells. We prioritize DDR2, STOM, and KANK2 as promising therapeutic targets in PSP with striking cross-species validations. We share our findings and data via our interactive application tool PSP RNAseq Atlas ( https://rtools.mayo.edu/PSP_RNAseq_Atlas/ ). Our findings reveal robust glial transcriptome changes in PSP, provide a cross-species systems biology approach, and a tool for therapeutic target discoveries in PSP with potential application in other neurodegenerative diseases.
MeSH term(s)	Humans ; Animals ; Mice ; Supranuclear Palsy, Progressive/pathology ; tau Proteins/metabolism ; Systems Biology ; Tauopathies/pathology ; Neuroglia/metabolism ; Discoidin Domain Receptor 2
Chemical Substances	tau Proteins ; DDR2 protein, human (EC 2.7.10.1) ; Discoidin Domain Receptor 2 (EC 2.7.10.1)
Language	English
Publishing date	2023-11-02
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-42626-3
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Article: Clinical Deep Phenotyping of

Campbell, Alana S / Ho, Charlotte C G / Atık, Merve / Allen, Mariet / Lincoln, Sarah / Malphrus, Kimberly / Nguyen, Thuy / Oatman, Stephanie R / Corda, Morgane / Conway, Olivia / Strickland, Samantha / Petersen, Ronald C / Dickson, Dennis W / Graff-Radford, Neill R / Ertekin-Taner, Nilüfer

Neurology. Genetics

2022 Volume 8, Issue 2, Page(s) e655

Abstract: Background and objectives: Putative loss-of-function (pLOF) : Methods: Genotypes were determined for 5,353 individuals evaluated at Mayo Clinic for 6 reported : Results: We confirmed that : Discussion: Our study provides a deep clinical review ... ...

Abstract	Background and objectives: Putative loss-of-function (pLOF) Methods: Genotypes were determined for 5,353 individuals evaluated at Mayo Clinic for 6 reported Results: We confirmed that Discussion: Our study provides a deep clinical review of phenotypic characteristics of mutation carriers for 6
Language	English
Publishing date	2022-01-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2818607-2
ISSN	2376-7839
ISSN	2376-7839
DOI	10.1212/NXG.0000000000000655
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Article ; Online: Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways.

Ibanez, Kristen R / McFarland, Karen N / Phillips, Jennifer / Allen, Mariet / Lessard, Christian B / Zobel, Lillian / De La Cruz, Elsa Gonzalez / Shah, Shivani / Vo, Quan / Wang, Xue / Quicksall, Zachary / Ryu, Daniel / Funk, Cory / Ertekin-Taner, Nilüfer / Prokop, Stefan / Golde, Todd E / Chakrabarty, Paramita

Alzheimer's research & therapy

2022 Volume 14, Issue 1, Page(s) 104

Abstract: Background: The S209F variant of Abelson Interactor Protein 3 (ABI3) increases risk for Alzheimer's disease (AD), but little is known about its function in relation to AD pathogenesis.: Methods: Here, we use a mouse model that is deficient in Abi3 ... ...

Abstract	Background: The S209F variant of Abelson Interactor Protein 3 (ABI3) increases risk for Alzheimer's disease (AD), but little is known about its function in relation to AD pathogenesis. Methods: Here, we use a mouse model that is deficient in Abi3 locus to study how the loss of function of Abi3 impacts two cardinal neuropathological hallmarks of AD-amyloid β plaques and tau pathology. Our study employs extensive neuropathological and transcriptomic characterization using transgenic mouse models and adeno-associated virus-mediated gene targeting strategies. Results: Analysis of bulk RNAseq data confirmed age-progressive increase in Abi3 levels in rodent models of AD-type amyloidosis and upregulation in AD patients relative to healthy controls. Using RNAscope in situ hybridization, we localized the cellular distribution of Abi3 in mouse and human brains, finding that Abi3 is expressed in both microglial and non-microglial cells. Next, we evaluated Abi3 Conclusions: These data provide an important experimental framework for understanding the role of Abi3-Gngt2 function and early inflammatory gliosis in AD. Our studies also demonstrate that inflammatory gliosis could have opposing effects on amyloid and tau pathology, highlighting the unpredictability of targeting immune pathways in AD.
MeSH term(s)	Animals ; Humans ; Mice ; Adaptor Proteins, Signal Transducing/genetics ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Amyloid beta-Protein Precursor/genetics ; Amyloidosis/genetics ; Brain/metabolism ; Disease Models, Animal ; Gliosis/metabolism ; GTP-Binding Protein gamma Subunits/genetics ; Membrane Glycoproteins/metabolism ; Mice, Transgenic ; Plaque, Amyloid/pathology ; Receptors, Immunologic/metabolism ; tau Proteins/genetics ; tau Proteins/metabolism
Chemical Substances	Abi-3 protein, mouse ; ABI3 protein, human ; Adaptor Proteins, Signal Transducing ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; GTP-Binding Protein gamma Subunits ; Membrane Glycoproteins ; Receptors, Immunologic ; tau Proteins ; Trem2 protein, mouse ; Gngt2 protein, mouse
Language	English
Publishing date	2022-07-27
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2506521-X
ISSN	1758-9193 ; 1758-9193
ISSN (online)	1758-9193
ISSN	1758-9193
DOI	10.1186/s13195-022-01044-1
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Article ; Online: Epigenomic features related to microglia are associated with attenuated effect of APOE ε4 on Alzheimer's disease risk in humans.

Ma, Yiyi / Yu, Lei / Olah, Marta / Smith, Rebecca / Oatman, Stephanie R / Allen, Mariet / Pishva, Ehsan / Zhang, Bin / Menon, Vilas / Ertekin-Taner, Nilüfer / Lunnon, Katie / Bennett, David A / Klein, Hans-Ulrich / De Jager, Philip L

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

2021 Volume 18, Issue 4, Page(s) 688–699

Abstract: Not all apolipoprotein E (APOE) ε4 carriers who survive to advanced age develop Alzheimer's disease (AD); factors attenuating the risk of ε4 on AD may exist. Guided by the top ε4-attenuating signals from methylome-wide association analyses (N = 572, ε4+ ... ...

Abstract	Not all apolipoprotein E (APOE) ε4 carriers who survive to advanced age develop Alzheimer's disease (AD); factors attenuating the risk of ε4 on AD may exist. Guided by the top ε4-attenuating signals from methylome-wide association analyses (N = 572, ε4+ and ε4-) of neurofibrillary tangles and neuritic plaques, we conducted a meta-analysis for pathological AD within the ε4+ subgroups (N = 235) across four independent collections of brains. Cortical RNA-seq and microglial morphology measurements were used in functional analyses. Three out of the four significant CpG dinucleotides were captured by one principal component (PC1), which interacts with ε4 on AD, and is associated with expression of innate immune genes and activated microglia. In ε4 carriers, reduction in each unit of PC1 attenuated the odds of AD by 58% (odds ratio = 2.39, 95% confidence interval = [1.64,3.46], P = 7.08 × 10
MeSH term(s)	Alleles ; Alzheimer Disease/pathology ; Apolipoprotein E4/genetics ; Apolipoproteins E/genetics ; Epigenomics ; Genotype ; Humans ; Microglia/pathology ; Neurofibrillary Tangles/pathology
Chemical Substances	Apolipoprotein E4 ; Apolipoproteins E
Language	English
Publishing date	2021-09-05
Publishing country	United States
Document type	Journal Article ; Meta-Analysis ; Research Support, N.I.H., Extramural
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.12425
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Article ; Online: Analysis of intraoperative human brain tissue transcriptome reveals putative risk genes and altered molecular pathways in glioma-related seizures.

Feyissa, Anteneh M / Carrano, Anna / Wang, Xue / Allen, Mariet / Ertekin-Taner, Nilüfer / Dickson, Dennis W / Jentoft, Mark E / Rosenfeld, Steven S / Tatum, William O / Ritaccio, Anthony L / Guerrero-Cázares, Hugo / Quiñones-Hinojosa, Alfredo

Epilepsy research

2021 Volume 173, Page(s) 106618

Abstract: Background: The pathogenesis of glioma-related seizures (GRS) is poorly understood. Here in, we aim to identify putative molecular pathways that lead to the development of GRS.: Methods: We determined brain transcriptome from intraoperative human ... ...

Abstract	Background: The pathogenesis of glioma-related seizures (GRS) is poorly understood. Here in, we aim to identify putative molecular pathways that lead to the development of GRS. Methods: We determined brain transcriptome from intraoperative human brain tissue of patients with either GRS, glioma without seizures (non-GRS), or with idiopathic temporal lobe epilepsy (iTLE). We performed transcriptome-wide comparisons between disease groups tissue from non-epileptic controls (non-EC) to identify differentially-expressed genes (DEG). We compared DEGs to identify those that are specific or common to the groups. Through a gene ontology analysis, we identified molecular pathways enriched for genes with a Log-fold change ≥1.5 or ≤-1.5 and p-value <0.05 compared to non-EC. Results: We identified 110 DEGs that are associated with GRS vs. non-GRS: 80 genes showed high and 30 low expression in GRS. There was significant overexpression of genes involved in cell-to-cell and glutamatergic signaling (CELF4, SLC17A7, and CAMK2A) and down-regulation of genes involved immune-trafficking (CXCL8, H19, and VEGFA). In the iTLE vs GRS analysis, there were 1098 DEGs: 786 genes were overexpressed and 312 genes were underexpressed in the GRS samples. There was significant enrichment for genes considered markers of oncogenesis (GSC, MYBL2, and TOP2A). Further, there was down-regulation of genes involved in the glutamatergic neurotransmission (vesicular glutamate transporter-2) in the GRS vs. iTLE samples. Conclusions: We identified a number of altered processes such as cell-to-cell signaling and interaction, inflammation-related, and glutamatergic neurotransmission in the pathogenesis of GRS. Our findings offer a new landscape of targets to further study in the fields of brain tumors and seizures.
MeSH term(s)	Brain/pathology ; Computational Biology ; Gene Expression Profiling ; Glioma/complications ; Glioma/genetics ; Glioma/surgery ; Humans ; Seizures/etiology ; Seizures/genetics ; Transcriptome
Language	English
Publishing date	2021-03-18
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	632939-1
ISSN	1872-6844 ; 0920-1211
ISSN (online)	1872-6844
ISSN	0920-1211
DOI	10.1016/j.eplepsyres.2021.106618
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Article ; Online: EPIGENOMIC FEATURES RELATED TO MICROGLIA ARE ASSOCIATED WITH ATTENUATED EFFECT OF APOE ε4 ON ALZHEIMER'S DISEASE RISK IN HUMANS.

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

2020 Volume 16, Issue Suppl 2

Abstract: ... Not ... ...

Abstract	Not all
MeSH term(s)	Aged ; Alleles ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Apolipoprotein E4/genetics ; Brain/pathology ; Epigenomics ; Female ; Genetic Predisposition to Disease ; Heterozygote ; Humans ; Male ; Microglia/metabolism
Chemical Substances	Apolipoprotein E4
Language	English
Publishing date	2020-12-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.043533
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