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Article ; Online: Lower levels of cortical [

Dean, Brian / Haroutunian, Vahram / Scarr, Elizabeth

2023 Volume 255, Page(s) 274–282

Abstract: Multiple lines of evidence argue for lower levels of cortical muscarinic M1 receptors (CHRM1) in people with schizophrenia which is possibly due to a sub-group within the disorder who have a marked loss of CHRM1 (muscarinic receptor deficit sub-group ( ... ...

Abstract	Multiple lines of evidence argue for lower levels of cortical muscarinic M1 receptors (CHRM1) in people with schizophrenia which is possibly due to a sub-group within the disorder who have a marked loss of CHRM1 (muscarinic receptor deficit sub-group (MRDS)). In this study we sought to determine if the lower levels of CHRM1 was apparent in older people with schizophrenia and whether the loss of CHRM1 was associated with symptom severity by measuring levels of cortical [
MeSH term(s)	Humans ; Aged ; Pirenzepine ; Schizophrenia/metabolism ; Receptor, Muscarinic M1/metabolism ; Cognition Disorders ; Cognition
Chemical Substances	Pirenzepine (3G0285N20N) ; Receptor, Muscarinic M1 ; CHRM1 protein, human
Language	English
Publishing date	2023-04-19
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639422-x
ISSN	1573-2509 ; 0920-9964
ISSN (online)	1573-2509
ISSN	0920-9964
DOI	10.1016/j.schres.2023.03.035
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Zs.MO 543: Show issues

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Article ; Online: Human apolipoprotein E isoforms are differentially sialylated and the sialic acid moiety in ApoE2 attenuates ApoE2-Aβ interaction and Aβ fibrillation.

Moon, Hee-Jung / Haroutunian, Vahram / Zhao, Liqin

Neurobiology of disease

2022 Volume 164, Page(s) 105631

Abstract: The APOE genotype is the most prominent genetic risk factor for the development of late-onset Alzheimer''s disease (LOAD); however, the underlying mechanisms remain unclear. In the present study, we found that the sialylation profiles of ApoE protein in ... ...

Abstract	The APOE genotype is the most prominent genetic risk factor for the development of late-onset Alzheimer''s disease (LOAD); however, the underlying mechanisms remain unclear. In the present study, we found that the sialylation profiles of ApoE protein in the human brain are significantly different among the three isoforms, with ApoE2 exhibiting the most abundant sialic acid modification whereas ApoE4 had the least. We further observed that the sialic acid moiety in ApoE2 significantly affected the interaction between ApoE2 and Aβ peptides. The removal of sialic acid in ApoE2 increased the ApoE2 binding affinity for the Aβ17-24 region of Aβ and promoted Aβ fibrillation. These findings provide a plausible explanation for the well-documented differential roles of ApoE isoforms in Aβ pathogenesis. Specifically, compared to the other two isotypes, the higher expression of sialic acid in ApoE2 may contribute to the less potent interaction between ApoE2 and Aβ and ultimately the slower rate of brain Aβ deposition, a mechanism thought to underlie ApoE2-mediated decreased risk for AD. Future studies are warranted to determine whether the differential sialylation in ApoE isoforms may also contribute to some of their other distinct properties, such as their divergent preferences in associations with lipids and lipoproteins, as well as their potential impact on neuroinflammation through modulation of microglial Siglec activity. Overall, our findings lead to the insight that the sialic acid structure is an important posttranslational modification (PTM) that alters ApoE protein functions with relevance for AD.
MeSH term(s)	Alzheimer Disease/metabolism ; Amyloid/metabolism ; Amyloid beta-Peptides/metabolism ; Apolipoproteins E/metabolism ; Brain/metabolism ; Humans ; N-Acetylneuraminic Acid/metabolism ; Protein Isoforms/metabolism
Chemical Substances	Amyloid ; Amyloid beta-Peptides ; Apolipoproteins E ; Protein Isoforms ; N-Acetylneuraminic Acid (GZP2782OP0)
Language	English
Publishing date	2022-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2022.105631
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Article ; Online: Up-Regulation of S100 Gene Family in Brain Samples of a Subgroup of Individuals with Schizophrenia: Meta-analysis.

Shamir, Anat / Yitzhaky, Assif / Segev, Aviv / Haroutunian, Vahram / Katsel, Pavel / Hertzberg, Libi

Neuromolecular medicine

2023 Volume 25, Issue 3, Page(s) 388–401

Abstract: The S100 proteins family is known to affect neuroinflammation and astrocyte activation, which have been suggested to be contributors to the pathogenesis of schizophrenia. We conducted a systematic meta-analysis of S100 genes differential expression in ... ...

Abstract	The S100 proteins family is known to affect neuroinflammation and astrocyte activation, which have been suggested to be contributors to the pathogenesis of schizophrenia. We conducted a systematic meta-analysis of S100 genes differential expression in postmortem samples of patients with schizophrenia vs. healthy controls, following the commonly used Preferred Reporting Items for Systematic Reviews and Meta-Analysis (PRISMA) guidelines. Twelve microarray datasets met the inclusion criteria (overall 511 samples, 253 schizophrenia and 258 controls were analyzed). Nine out of 21 genes were significantly up-regulated or with tendency for up-regulation. A per-sample fold change analysis indicated that the S100 genes' up-regulation was concentrated in a subgroup of the patients. None of the genes have been found to be down-regulated. ANXA3, which encodes Annexin 3 protein and was associated with neuroinflammation, was up-regulated and positively correlated with the S100 genes' expression pattern. In addition, astrocytes and endothelial cell markers were significantly correlated with S100A8 expression. S100 correlation with ANXA3 and endothelial cell markers suggests that the up-regulation we detected reflects increased inflammation. However, it might also reflect astrocytes abundance or activation. The fact that S100 proteins were shown to be up-regulated in blood samples and other body fluids of patients with schizophrenia suggests a potential role as biomarkers, which might help disease subtyping, and the development of etiological treatments for immune dysregulation in schizophrenia.
MeSH term(s)	Humans ; Up-Regulation ; Schizophrenia/genetics ; Neuroinflammatory Diseases ; Brain/metabolism ; S100 Proteins/genetics ; S100 Proteins/metabolism
Chemical Substances	S100 Proteins
Language	English
Publishing date	2023-04-02
Publishing country	United States
Document type	Meta-Analysis ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2077809-0
ISSN	1559-1174 ; 1535-1084
ISSN (online)	1559-1174
ISSN	1535-1084
DOI	10.1007/s12017-023-08743-4
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Article ; Online: Is Alzheimer disease a failure of mobilizing immune defense? Lessons from cognitively fit oldest-old.

Katsel, Pavel / Haroutunian, Vahram

Dialogues in clinical neuroscience

2019 Volume 21, Issue 1, Page(s) 7–19

Abstract: Multifaceted evidence supports the hypothesis that inflammatory-immune mechanisms contribute to Alzheimer disease (AD) neuropathology and genetic association of several immune specific genes (TREM2, CR1, and CD33) suggests that maladaptive immune ... ...

Abstract	Multifaceted evidence supports the hypothesis that inflammatory-immune mechanisms contribute to Alzheimer disease (AD) neuropathology and genetic association of several immune specific genes (TREM2, CR1, and CD33) suggests that maladaptive immune responses may be pivotal drivers of AD pathogenesis. We reviewed microglia-related data from postmortem AD studies and examined supporting evidence from AD animal models to answer the following questions: i) What is the temporal sequence of immune activation in AD progression and what is its impact on cognition? ii) Are there discordant, "primed", microglia responses in AD vs successful cognitive aging? iii) Does central nervous system (CNS) repair in aging depend on recruitment of the elements of cellular adaptive immune response such as effector T cells, and can the recruitment of systemic immune cells ameliorate AD neuropathology? iv) How effective are the immune-system-based therapeutic approaches currently employed for the treatment of AD?
MeSH term(s)	Adaptive Immunity/immunology ; Aged, 80 and over ; Alzheimer Disease/complications ; Alzheimer Disease/immunology ; Alzheimer Disease/psychology ; Cognition ; Cognitive Aging ; Encephalitis/complications ; Encephalitis/immunology ; Humans ; Microglia/immunology
Language	English
Publishing date	2019-10-10
Publishing country	France
Document type	Journal Article
ZDB-ID	2188781-0
ISSN	1958-5969 ; 1294-8322
ISSN (online)	1958-5969
ISSN	1294-8322
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Zs.A 6188: Show issues

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Article ; Online: Role of cumulative biological risk in mediating socioeconomic disparities in cognitive function in the elderly: a mediation analysis.

Akrivos, Jimmy / Zhu, Carolyn Wei / Haroutunian, Vahram

BMJ open

2020 Volume 10, Issue 9, Page(s) e035847

Abstract: Objectives: To evaluate whether allostatic load (AL), a measure of cumulative biological risk, fully or partially mediates observed socioeconomic status (SES) differences in cognitive function in the elderly.: Design: Cross-sectional mediation ... ...

Abstract	Objectives: To evaluate whether allostatic load (AL), a measure of cumulative biological risk, fully or partially mediates observed socioeconomic status (SES) differences in cognitive function in the elderly. Design: Cross-sectional mediation analysis. Setting: Community-dwelling US elderly who participated in the National Health and Nutrition Examination Survey (NHANES). Participants: The NHANES uses a complex, multistage, probability sampling design to select a nationally representative sample. Of the 4976 elderly (60 years or older) who were selected, 3234 agreed to participate in the household and medical exam interviews (65% response rate). Primary and secondary outcome measures: Performance on the Digit Symbol Substitution Test (DSST)-a measure of cognitive function. Results: Relative to participants with the lowest level of education or family income, participants who were college graduates (β=24.4, 95% CI 22 to 26.8, p<0.0001) or in the highest income quartile (β=17.3, 95% CI 15.2 to 19.4, p<0.0001) had the highest DSST scores and the least AL burden (β=-0.72, 95% CI -0.98 to -0.47 and β=-0.82, 95% CI -1 to -0.57; p<0.0001, respectively). Although, AL was significantly negatively associated with cognitive performance (β = -1, 95% CI -1.4 to -0.5, p<0.0001), it mediated at most 4.5% of the SES effect on DSST performance. Conclusions: The findings suggest that AL, as measured by a summary index of parameters for cardiovascular function, metabolism and chronic inflammation, is not a significant mediator of SES-related differences in cognitive function in the elderly. Further efforts are required to elucidate the exact physiological pathways and mechanisms through which SES impacts cognitive function in late life.
MeSH term(s)	Aged ; Cognition ; Cross-Sectional Studies ; Educational Status ; Humans ; Mediation Analysis ; Nutrition Surveys
Language	English
Publishing date	2020-09-18
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2599832-8
ISSN	2044-6055 ; 2044-6055
ISSN (online)	2044-6055
ISSN	2044-6055
DOI	10.1136/bmjopen-2019-035847
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Article: Human Brain and Serum Advanced Glycation End Products are Highly Correlated: Preliminary Results of Their Role in Alzheimer Disease and Type 2 Diabetes.

Beeri, Michal Schnaider / Uribarri, Jaime / Cai, Weijing / Buchman, Aron S / Haroutunian, Vahram

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists

2021 Volume 26, Issue 5, Page(s) 576–577

MeSH term(s)	Alzheimer Disease ; Brain ; Diabetes Mellitus, Type 2 ; Glycation End Products, Advanced ; Humans
Chemical Substances	Glycation End Products, Advanced
Language	English
Publishing date	2021-02-09
Publishing country	United States
Document type	Letter
ZDB-ID	1473503-9
ISSN	1530-891X
ISSN	1530-891X
DOI	10.4158/1934-2403-26.5.576
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Article: Alzheimer's disease transcriptional landscape in ex-vivo human microglia.

Roussos, Panos / Kosoy, Roman / Fullard, John / Bendl, Jaroslav / Kleopoulos, Steven / Shao, Zhiping / Argyriou, Stathis / Mathur, Deepika / Vicari, James / Ma, Yixuan / Humphrey, Jack / Brophy, Erica / Raj, Towfique / Katsel, Pavel / Voloudakis, Georgios / Lee, Donghoon / Bennett, David / Haroutunian, Vahram / Hoffman, Gabriel

Research square

2024

Abstract: Microglia are resident immune cells of the brain and are implicated in the etiology of Alzheimer's Disease (AD) and other diseases. Yet the cellular and molecular processes regulating their function throughout the course of the disease are poorly ... ...

Abstract	Microglia are resident immune cells of the brain and are implicated in the etiology of Alzheimer's Disease (AD) and other diseases. Yet the cellular and molecular processes regulating their function throughout the course of the disease are poorly understood. Here, we present the transcriptional landscape of primary microglia from 189 human postmortem brains, including 58 healthy aging individuals and 131 with a range of disease phenotypes, including 63 patients representing the full spectrum of clinical and pathological severity of AD. We identified transcriptional changes associated with multiple AD phenotypes, capturing the severity of dementia and neuropathological lesions. Transcript-level analyses identified additional genes with heterogeneous isoform usage and AD phenotypes. We identified changes in gene-gene coordination in AD, dysregulation of co-expression modules, and disease subtypes with distinct gene expression. Taken together, these data further our understanding of the key role of microglia in AD biology and nominate candidates for therapeutic intervention.
Language	English
Publishing date	2024-01-26
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3851590/v1
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Article: Schizophrenia: susceptibility genes and oligodendroglial and myelin related abnormalities.

Roussos, Panos / Haroutunian, Vahram

Frontiers in cellular neuroscience

2014 Volume 8, Page(s) 5

Abstract: Given that the genetic risk for schizophrenia is highly polygenic and the effect sizes, even for rare or de novo events, are modest at best, it has been suggested that multiple biological pathways are likely to be involved in the etiopathogenesis of the ... ...

Abstract	Given that the genetic risk for schizophrenia is highly polygenic and the effect sizes, even for rare or de novo events, are modest at best, it has been suggested that multiple biological pathways are likely to be involved in the etiopathogenesis of the disease. Most efforts in understanding the cellular basis of schizophrenia have followed a "neuron-centric" approach, focusing on alterations in neurotransmitter systems and synapse cytoarchitecture. However, multiple lines of evidence coming from genetics and systems biology approaches suggest that apart from neurons, oligodendrocytes and potentially other glia are affected from schizophrenia risk loci. Neurobiological abnormalities linked with genetic association signal could identify abnormalities that are more likely to be primary, versus environmentally induced changes or downstream events. Here, we summarize genetic data that support the involvement of oligodendrocytes in schizophrenia, providing additional evidence for a causal role with the disease. Given the undeniable evidence of both neuronal and glial abnormalities in schizophrenia, we propose a neuro-glial model that invokes abnormalities at the node of Ranvier as a functional unit in the etiopathogenesis of the disease.
Language	English
Publishing date	2014-01-21
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2014.00005
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Article: Efficient differential expression analysis of large-scale single cell transcriptomics data using dreamlet.

Hoffman, Gabriel E / Lee, Donghoon / Bendl, Jaroslav / Fnu, Prashant / Hong, Aram / Casey, Clara / Alvia, Marcela / Shao, Zhiping / Argyriou, Stathis / Therrien, Karen / Venkatesh, Sanan / Voloudakis, Georgios / Haroutunian, Vahram / Fullard, John F / Roussos, Panos

Research square

2023

Abstract: Advances in single-cell and -nucleus transcriptomics have enabled generation of increasingly large-scale datasets from hundreds of subjects and millions of cells. These studies promise to give unprecedented insight into the cell type specific biology of ... ...

Abstract	Advances in single-cell and -nucleus transcriptomics have enabled generation of increasingly large-scale datasets from hundreds of subjects and millions of cells. These studies promise to give unprecedented insight into the cell type specific biology of human disease. Yet performing differential expression analyses across subjects remains difficult due to challenges in statistical modeling of these complex studies and scaling analyses to large datasets. Our open-source R package dreamlet (DiseaseNeurogenomics.github.io/dreamlet) uses a pseudobulk approach based on precision-weighted linear mixed models to identify genes differentially expressed with traits across subjects for each cell cluster. Designed for data from large cohorts, dreamlet is substantially faster and uses less memory than existing workflows, while supporting complex statistical models and controlling the false positive rate. We demonstrate computational and statistical performance on published datasets, and a novel dataset of 1.4M single nuclei from postmortem brains of 150 Alzheimer's disease cases and 149 controls.
Language	English
Publishing date	2023-05-02
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-2705625/v1
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Article: ApoE Alzheimer's Disease Aβ-amyloid plaque morphology varies according to APOE isotype.

Caesar, Ina / Nilsson, K Peter R / Hammarstrom, Per / Lindgren, Mikael / Prokop, Stefan / Heppner, Frank L / Schmeidler, James / Haroutunian, Vahram / Holtzman, David M / Hof, Patrick R / Gandy, Sam

Research square

2023

Abstract: Background: The apolipoprotein E (: Methods: We have employed hyperspectral fluorescence imaging with an amyloidspecific, conformation-sensing probe, p-FTAA, to elucidate protein aggregate structure and morphology in fresh frozen prefrontal cortex ... ...

Abstract	Background: The apolipoprotein E ( Methods: We have employed hyperspectral fluorescence imaging with an amyloidspecific, conformation-sensing probe, p-FTAA, to elucidate protein aggregate structure and morphology in fresh frozen prefrontal cortex samples from human postmortem AD brain tissue samples from patients homozygous for either Results: As expected Conclusions: These data support the hypothesis that one mechanism by which the
Language	English
Publishing date	2023-02-08
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-2524641/v1
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