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      The Role of TREM2 in Alzheimer’s Disease and Other Neurological Disorders

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          Abstract

          Alzheimer’s disease (AD) is the leading cause of dementia worldwide. Late-onset AD (LOAD), is the most common form of Alzheimer’s disease, representing about >95% of cases and early-onset AD represents <5% of cases. Several risk factors have been discovered that are associated with AD, with advancing age being the most prominent. Other environmental risk factors include diabetes mellitus, level of physical activity, educational status, hypertension and head injury. The most well known genetic risk factor for LOAD is inheritance of the apolipoprotein (apo) E4 allele. Recently, rare variants of TREM2 have been reported as a significant risk factor for LOAD, comparable to inheritance of apoE4. In this review we will focus on the role(s) of TREM2 in AD as well as in other neurodegenerative disorders.

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          The Microglial Sensome Revealed by Direct RNA Sequencing

          Suzanne E Hickman, Nathan D. Kingery, Toshiro K Ohsumi … (2013)
          Microglia, the principal neuroimmune sentinels of the brain, continuously sense changes in their environment and respond to invading pathogens, toxins and cellular debris. Microglia exhibit plasticity and can assume neurotoxic or neuroprotective priming states that determine their responses to danger. We used direct RNA sequencing, without amplification or cDNA synthesis, to determine the quantitative transcriptomes of microglia of healthy adult and aged mice. We validated our findings by fluorescent dual in-situ hybridization, unbiased proteomic analysis and quantitative PCR. We report here that microglia have a distinct transcriptomic signature and express a unique cluster of transcripts encoding proteins for sensing endogenous ligands and microbes that we term the “sensome”. With aging, sensome transcripts for endogenous ligand recognition are downregulated, whereas those involved in microbe recognition and host defense are upregulated. In addition, aging is associated with an overall increase in expression of microglial genes involved in neuroprotection.
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            Cutting edge: inflammatory responses can be triggered by TREM-1, a novel receptor expressed on neutrophils and monocytes.

            A Bouchon, J. Dietrich, M Colonna (2000)
            We have identified new activating receptors of the Ig superfamily expressed on human myeloid cells, called TREM (triggering receptor expressed on myeloid cells). TREM-1 is selectively expressed on blood neutrophils and a subset of monocytes and is up-regulated by bacterial LPS. Engagement of TREM-1 triggers secretion of IL-8, monocyte chemotactic protein-1, and TNF-alpha and induces neutrophil degranulation. Intracellularly, TREM-1 induces Ca2+ mobilization and tyrosine phosphorylation of extracellular signal-related kinase 1 (ERK1), ERK2 and phospholipase C-gamma. To mediate activation, TREM-1 associates with the transmembrane adapter molecule DAP12. Thus, TREM-1 mediates activation of neutrophil and monocytes, and may have a predominant role in inflammatory responses.
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              Cutting edge: TREM-2 attenuates macrophage activation.

              Isaiah Turnbull, Susan Gilfillan, Marina Cella … (2006)
              The triggering receptor expressed on myeloid cells 2 (TREM-2) delivers intracellular signals through the adaptor DAP12 to regulate myeloid cell function both within and outside the immune system. The role of TREM-2 in immunity has been obscured by the failure to detect expression of the TREM-2 protein in vivo. In this study, we show that TREM-2 is expressed on macrophages infiltrating the tissues from the circulation and that alternative activation with IL-4 can induce TREM-2. TREM-2 expression is abrogated by macrophage maturation with LPS of IFN-gamma. Using TREM-2(-/-) mice, we find that TREM-2 functions to inhibit cytokine production by macrophages in response to the TLR ligands LPS, zymosan, and CpG. Furthermore, we find that TREM-2 completely accounts for the increased cytokine production previously reported by DAP12(-/-) macrophages. Taken together, these data show that TREM-2 is expressed on newly differentiated and alternatively activated macrophages and functions to restrain macrophage activation.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101587593
                Journal ID (pubmed-jr-id): 40437
                Journal ID (nlm-ta): J Alzheimers Dis Parkinsonism
                Journal ID (iso-abbrev): J Alzheimers Dis Parkinsonism
                Title: Journal of Alzheimer's disease & Parkinsonism
                ISSN (Electronic): 2161-0460
                Publication date Nihms-submitted: 27 January 2015
                Publication date (Electronic): 6 October 2014
                Publication date (Print): November 2014
                Publication date PMC-release: 04 February 2015
                Volume: 4
                Issue: 5
                Electronic Location Identifier: 160
                Affiliations
                [1 ]Departments of Neurology, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, USA
                [2 ]Pathology, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, USA
                [3 ]Psychiatry, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY 10016, USA
                [4 ]Physiology and Neuroscience, New York University School of Medicine, Alexandria ERSP, 450 East 29th Street, New York, NY10016, USA
                [5 ]King Abdulaziz University, School of Medicine, Jeddah, Saudi Arabia
                Author notes
                [* ] Corresponding author: Thomas Wisniewski, New York University School of Medicine, Alexandria ERSP, Rm 802, 450 East 29th St. New York, NY 10016, USA, Tel: (212) 263-7993; Fax: (212) 263-7528; thomas.wisniewski@ 123456nyumc.org
                Article
                Manuscript ID: NIHMS658559
                DOI: 10.4172/2161-0460.1000160
                PMC ID: 4317331
                SO-VID: 4fbf54a4-9f95-446f-95a6-e27b0a08347d
                Copyright © Copyright: © 2014 Yaghmoor F, et al.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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                Subject: Article

                Keywords: trem-2,alzheimer’s disease,fronto-temporal dementia,nasu-hakola disease,hereditary diffused leukoencephalopathy with spheroids,parkinson’s disease,amyotrophic lateral sclerosis
                Data availability:
                Keywords: trem-2, alzheimer’s disease, fronto-temporal dementia, nasu-hakola disease, hereditary diffused leukoencephalopathy with spheroids, parkinson’s disease, amyotrophic lateral sclerosis

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