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Article ; Online: Emerging blood-based biomarkers for Alzheimer disease.

Bekris, Lynn M / Leverenz, James B

2020 Volume 87, Issue 9, Page(s) 537–539

MeSH term(s)	Aged ; Aged, 80 and over ; Alzheimer Disease/diagnosis ; Amyloid beta-Peptides/blood ; Biomarkers/blood ; Female ; Humans ; Male ; Phosphorylation ; tau Proteins/blood
Chemical Substances	Amyloid beta-Peptides ; Biomarkers ; MAPT protein, human ; tau Proteins
Language	English
Publishing date	2020-08-31
Publishing country	United States
Document type	Journal Article
ZDB-ID	639116-3
ISSN	1939-2869 ; 0891-1150
ISSN (online)	1939-2869
ISSN	0891-1150
DOI	10.3949/ccjm.87a.20133
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Article ; Online: Potential role of miRNA-140 in Alzheimer's disease.

Akhter, Rumana / Bekris, Lynn M

Aging

2019 Volume 11, Issue 4, Page(s) 1087–1088

MeSH term(s)	Alzheimer Disease/metabolism ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism
Chemical Substances	MicroRNAs ; Mirn140 microRNA, human
Language	English
Publishing date	2019-02-19
Publishing country	United States
Document type	Editorial
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.101827
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Article ; Online: TREM2 alters the phagocytic, apoptotic and inflammatory response to Aβ

Akhter, Rumana / Shao, Yvonne / Formica, Shane / Khrestian, Maria / Bekris, Lynn M

Molecular immunology

2021 Volume 131, Page(s) 171–179

Abstract: Alzheimer's disease (AD) is characterized by the accumulation in the brain of extracellular amyloid β (Aβ) plaques as well as intraneuronal inclusions (neurofibrillary tangles) consisting of total tau and phosphorylated tau. Also present are dystrophic ... ...

Abstract	Alzheimer's disease (AD) is characterized by the accumulation in the brain of extracellular amyloid β (Aβ) plaques as well as intraneuronal inclusions (neurofibrillary tangles) consisting of total tau and phosphorylated tau. Also present are dystrophic neurites, loss of synapses, neuronal death, and gliosis. AD genetic studies have highlighted the importance of inflammation in this disease by identifying several risk associated immune response genes, including TREM2. TREM2 has been strongly implicated in basic microglia function including, phagocytosis, apoptosis, and the inflammatory response to Aβ in mouse brain and primary cells. These studies show that microglia are key players in the response to Aβ and in the accumulation of AD pathology. However, details are still missing about which apoptotic or inflammatory factors rely on TREM2 in their response to Aβ, especially in human cell lines. Given these previous findings our hypothesis is that TREM2 influences the response to Aβ toxicity by enhancing phagocytosis and inhibiting both the BCL-2 family of apoptotic proteins and pro-inflammatory cytokines. Aβ
MeSH term(s)	Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Apoptosis/physiology ; Brain/metabolism ; Cell Line ; Cell Line, Tumor ; Hep G2 Cells ; Humans ; Inflammation/metabolism ; Membrane Glycoproteins/metabolism ; Microglia/metabolism ; Phagocytes/metabolism ; Phagocytosis/physiology ; Plaque, Amyloid/metabolism ; Receptors, Immunologic/metabolism ; THP-1 Cells ; U937 Cells
Chemical Substances	Amyloid beta-Peptides ; Membrane Glycoproteins ; Receptors, Immunologic ; TREM2 protein, human
Language	English
Publishing date	2021-01-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2020.12.035
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Article: Temporal Ordering of Inflammatory Analytes sTNFR2 and sTREM2 in Relation to Alzheimer's Disease Biomarkers and Clinical Outcomes.

Pillai, Jagan A / Khrestian, Maria / Bena, James / Leverenz, James B / Bekris, Lynn M

Frontiers in aging neuroscience

2021 Volume 13, Page(s) 676744

Abstract: Inflammatory changes are among the key markers of Alzheimer's disease (AD) related pathological changes. Pro-inflammatory analytes have been related to cognitive decline while others have been related to attenuating neuronal death. Among them, changes in ...

Abstract	Inflammatory changes are among the key markers of Alzheimer's disease (AD) related pathological changes. Pro-inflammatory analytes have been related to cognitive decline while others have been related to attenuating neuronal death. Among them, changes in cerebrospinal fluid (CSF) levels of soluble triggering receptor expressed on myeloid cells 2 (sTREM2) and soluble tumor necrosis factor receptor 2 (sTNFR2) have been described as impacting favorable clinical outcomes in AD. We therefore evaluate the effect of CSF sTREM2 and sTNFR2 when taken together on AD biomarkers and longitudinal clinical decline to understand their relative role on impacting AD clinical biomarkers and subsequent clinical outcomes. This longitudinal observational cohort study included 168 amyloid-positive (A+) and p-tau-positive (T+) participants with mild cognitive impairment (MCI) or AD dementia from the Alzheimer's Disease Neuroimaging Initiative (ADNI) with 109 of them having concomitant CSF sTREM2 and sTNFR2 data and 48 A+ T+ participants with MCI from a tertiary memory clinic cohort. An exploratory analysis was performed using data from 86 cognitively normal (CN) participants from ADNI with 72 of them having concomitant CSF AD biomarkers and CSF sTREM2 and sTNFR2 data. General linear models were used to evaluate the effect of sTREM2 and sTNFR2 levels on baseline CSF Aβ42, t-tau, and p-tau, and a linear mixed-effects model was used to assess longitudinal cognitive change after controlling for well-known covariates. Among ADNI A+ T+ MCI and AD dementia participants, CSF sTNFR2 had a stronger association, than CSF sTREM2, with CSF t-tau and p-tau. This was replicated among A+ T+ MCI participants from the memory clinic cohort. On the contrary, among A+ T+ CN participants, CSF sTREM2 explained significant variance in CSF t-tau and p-tau, while CSF sTNFR2 did not. When the effects of CSF sTNFR2 and t-tau on longitudinal cognitive change were taken into account, higher CSF sTREM2 predicted slower cognitive decline in A+ T+ AD dementia participants and faster decline in A+ T+ CN participants. Our results show that given the dynamic changes in sTREM2 and sTNFR2, the clinical impact of these distinct inflammation related biomarkers in tracking AD temporal progression across disease stages are likely to differ.
Language	English
Publishing date	2021-06-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2021.676744
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Article: TNFRSF1B

Pillai, Jagan A / Bebek, Gurkan / Khrestian, Maria / Bena, James / Bergmann, Cornelia C / Bush, William S / Leverenz, James B / Bekris, Lynn M

Frontiers in aging neuroscience

2021 Volume 13, Page(s) 638922

Abstract: Tumor necrosis factor receptor 2 (TNFR2) promotes neuronal survival downstream. This longitudinal study evaluated whether ... ...

Abstract	Tumor necrosis factor receptor 2 (TNFR2) promotes neuronal survival downstream. This longitudinal study evaluated whether the
Language	English
Publishing date	2021-02-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2558898-9
ISSN	1663-4365
ISSN	1663-4365
DOI	10.3389/fnagi.2021.638922
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Article ; Online: The biomarker and therapeutic potential of miRNA in Alzheimer's disease.

Bekris, Lynn M / Leverenz, James B

Neurodegenerative disease management

2015 Volume 5, Issue 1, Page(s) 61–74

Abstract: Alzheimer's disease (AD) is the most common cause of dementia. Currently, a clinical diagnosis of AD is based on evidence of both cognitive and functional decline. Progression is monitored by detailed clinical evaluations over many months to years. It is ...

Abstract	Alzheimer's disease (AD) is the most common cause of dementia. Currently, a clinical diagnosis of AD is based on evidence of both cognitive and functional decline. Progression is monitored by detailed clinical evaluations over many months to years. It is increasingly clear that to advance disease-modifying therapies for AD, patients must be identified and treated early, before obvious cognitive and functional changes. In addition, better methods are needed to sensitively monitor progression of disease and therapeutic efficacy. Therefore, considerable research has focused on characterizing biomarkers that can identify the disease early as well as accurately monitor disease progression. miRNA offer a unique opportunity for biomarker development. Here, we review research focused on characterizing miRNA as potential biomarkers and as a treatment for disease.
MeSH term(s)	Alzheimer Disease/diagnosis ; Alzheimer Disease/metabolism ; Alzheimer Disease/therapy ; Animals ; Biomarkers/metabolism ; Humans ; MicroRNAs/metabolism ; MicroRNAs/therapeutic use
Chemical Substances	Biomarkers ; MicroRNAs
Language	English
Publishing date	2015
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	1758-2032
ISSN (online)	1758-2032
DOI	10.2217/nmt.14.52
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Article ; Online: Amyloid Precursor Protein Variant, E665D, Associated With Unique Clinical and Biomarker Phenotype.

Abbatemarco, Justin R / Jones, Stephen E / Larvie, Mykol / Bekris, Lynn M / Khrestian, Maria E / Krishnan, Kamini / Leverenz, James B

American journal of Alzheimer's disease and other dementias

2021 Volume 36, Page(s) 1533317520981225

Abstract: We describe a clinical, imaging and biomarker phenotype associated with an amyloid precursor ... ...

Abstract	We describe a clinical, imaging and biomarker phenotype associated with an amyloid precursor gene
MeSH term(s)	Alzheimer Disease/genetics ; Amyloid beta-Peptides ; Amyloid beta-Protein Precursor/genetics ; Biomarkers ; Cerebral Amyloid Angiopathy ; Humans ; Male ; Middle Aged ; Phenotype
Chemical Substances	Amyloid beta-Peptides ; Amyloid beta-Protein Precursor ; Biomarkers
Language	English
Publishing date	2021-01-15
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1283069-0
ISSN	1938-2731 ; 0895-5336 ; 1082-5207 ; 1533-3175
ISSN (online)	1938-2731
ISSN	0895-5336 ; 1082-5207 ; 1533-3175
DOI	10.1177/1533317520981225
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Article ; Online: AlzGPS: a genome-wide positioning systems platform to catalyze multi-omics for Alzheimer's drug discovery.

Zhou, Yadi / Fang, Jiansong / Bekris, Lynn M / Kim, Young Heon / Pieper, Andrew A / Leverenz, James B / Cummings, Jeffrey / Cheng, Feixiong

Alzheimer's research & therapy

2021 Volume 13, Issue 1, Page(s) 24

Abstract: Background: Recent DNA/RNA sequencing and other multi-omics technologies have advanced the understanding of the biology and pathophysiology of AD, yet there is still a lack of disease-modifying treatments for AD. A new approach to integration of the ... ...

Abstract	Background: Recent DNA/RNA sequencing and other multi-omics technologies have advanced the understanding of the biology and pathophysiology of AD, yet there is still a lack of disease-modifying treatments for AD. A new approach to integration of the genome, transcriptome, proteome, and human interactome in the drug discovery and development process is essential for this endeavor. Methods: In this study, we developed AlzGPS (Genome-wide Positioning Systems platform for Alzheimer's Drug Discovery, https://alzgps.lerner.ccf.org ), a comprehensive systems biology tool to enable searching, visualizing, and analyzing multi-omics, various types of heterogeneous biological networks, and clinical databases for target identification and development of effective prevention and treatment for AD. Results: Via AlzGPS: (1) we curated more than 100 AD multi-omics data sets capturing DNA, RNA, protein, and small molecule profiles underlying AD pathogenesis (e.g., early vs. late stage and tau or amyloid endophenotype); (2) we constructed endophenotype disease modules by incorporating multi-omics findings and human protein-protein interactome networks; (3) we provided possible treatment information from ~ 3000 FDA approved/investigational drugs for AD using state-of-the-art network proximity analyses; (4) we curated nearly 300 literature references for high-confidence drug candidates; (5) we included information from over 1000 AD clinical trials noting drug's mechanisms-of-action and primary drug targets, and linking them to our integrated multi-omics view for targets and network analysis results for the drugs; (6) we implemented a highly interactive web interface for database browsing and network visualization. Conclusions: Network visualization enabled by AlzGPS includes brain-specific neighborhood networks for genes-of-interest, endophenotype disease module networks for omics-of-interest, and mechanism-of-action networks for drugs targeting disease modules. By virtue of combining systems pharmacology and network-based integrative analysis of multi-omics data, AlzGPS offers actionable systems biology tools for accelerating therapeutic development in AD.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/genetics ; Drug Discovery ; Humans ; Proteome ; Systems Biology ; Transcriptome
Chemical Substances	Proteome
Language	English
Publishing date	2021-01-13
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/s13195-020-00760-w
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Article ; Online: Peripheral sTREM2-Related Inflammatory Activity Alterations in Early-Stage Alzheimer's Disease.

Weber, Grace E / Khrestian, Maria / Tuason, Elizabeth D / Shao, Yvonne / Pillai, Jagan / Rao, Stephen / Feng, Hao / Zhou, Yadi / Cheng, Feixiong / DeSilva, Tara M / Stauffer, Shaun / Leverenz, James B / Bekris, Lynn M

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 208, Issue 10, Page(s) 2283–2299

Abstract: Alzheimer's disease (AD) has been linked to multiple immune system-related genetic variants. Triggering receptor expressed on myeloid cells 2 (TREM2) genetic variants are risk factors for AD and other neurodegenerative diseases. In addition, soluble ... ...

Abstract	Alzheimer's disease (AD) has been linked to multiple immune system-related genetic variants. Triggering receptor expressed on myeloid cells 2 (TREM2) genetic variants are risk factors for AD and other neurodegenerative diseases. In addition, soluble TREM2 (sTREM2) isoform is elevated in cerebrospinal fluid in the early stages of AD and is associated with slower cognitive decline in a disease stage-dependent manner. Multiple studies have reported an altered peripheral immune response in AD. However, less is known about the relationship between peripheral sTREM2 and an altered peripheral immune response in AD. The objective of this study was to explore the relationship between human plasma sTREM2 and inflammatory activity in AD. The hypothesis of this exploratory study was that sTREM2-related inflammatory activity differs by AD stage. We observed different patterns of inflammatory activity across AD stages that implicate early-stage alterations in peripheral sTREM2-related inflammatory activity in AD. Notably, fractalkine showed a significant relationship with sTREM2 across different analyses in the control groups that was lost in later AD-related stages with high levels in mild cognitive impairment. Although multiple other inflammatory factors either differed significantly between groups or were significantly correlated with sTREM2 within specific groups, three inflammatory factors (fibroblast growth factor-2, GM-CSF, and IL-1β) are notable because they exhibited both lower levels in AD, compared with mild cognitive impairment, and a change in the relationship with sTREM2. This evidence provides important support to the hypothesis that sTREM2-related inflammatory activity alterations are AD stage specific and provides critical information for therapeutic strategies focused on the immune response.
MeSH term(s)	Alzheimer Disease/genetics ; Biomarkers ; Humans
Chemical Substances	Biomarkers
Language	English
Publishing date	2022-05-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2100771
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Article ; Online: Multimodal single-cell/nucleus RNA sequencing data analysis uncovers molecular networks between disease-associated microglia and astrocytes with implications for drug repurposing in Alzheimer's disease.

Xu, Jielin / Zhang, Pengyue / Huang, Yin / Zhou, Yadi / Hou, Yuan / Bekris, Lynn M / Lathia, Justin / Chiang, Chien-Wei / Li, Lang / Pieper, Andrew A / Leverenz, James B / Cummings, Jeffrey / Cheng, Feixiong

Genome research

2021 Volume 31, Issue 10, Page(s) 1900–1912

Abstract: Because disease-associated microglia (DAM) and disease-associated astrocytes (DAA) are involved in the pathophysiology of Alzheimer's disease (AD), we systematically identified molecular networks between DAM and DAA to uncover novel therapeutic targets ... ...

Abstract	Because disease-associated microglia (DAM) and disease-associated astrocytes (DAA) are involved in the pathophysiology of Alzheimer's disease (AD), we systematically identified molecular networks between DAM and DAA to uncover novel therapeutic targets for AD. Specifically, we develop a network-based methodology that leverages single-cell/nucleus RNA sequencing data from both transgenic mouse models and AD patient brains, as well as drug-target network, metabolite-enzyme associations, the human protein-protein interactome, and large-scale longitudinal patient data. Through this approach, we find both common and unique gene network regulators between DAM (i.e.,
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/genetics ; Animals ; Astrocytes/metabolism ; Data Analysis ; Drug Repositioning ; Humans ; Mice ; Microglia/metabolism ; Retrospective Studies ; Sequence Analysis, RNA
Language	English
Publishing date	2021-02-24
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1284872-4
ISSN	1549-5469 ; 1088-9051 ; 1054-9803
ISSN (online)	1549-5469
ISSN	1088-9051 ; 1054-9803
DOI	10.1101/gr.272484.120
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