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  1. Article: Retromer Dysfunction and Neurodegenerative Disease.

    Reitz, Christiane

    Current genomics

    2018  Volume 19, Issue 4, Page(s) 279–288

    Abstract: In recent years, genomic, animal and cell biology studies have implicated deficiencies in retromer-mediated trafficking of proteins in an increasing number of neurodegenerative diseases including Alzheimer's Disease (AD), Parkinson's Disease (PD) and ... ...

    Abstract In recent years, genomic, animal and cell biology studies have implicated deficiencies in retromer-mediated trafficking of proteins in an increasing number of neurodegenerative diseases including Alzheimer's Disease (AD), Parkinson's Disease (PD) and Frontotemporal Lobar Degener-ation (FTLD). The retromer complex, which is highly conserved across all eukaryotes, regulates the sorting of transmembrane proteins out of endo-somes to the cell surface or to the trans-Golgi network. Within retromer, cargo selection and binding are performed by a trimer of the Vps26, Vps29 and Vps35 proteins, named the "Cargo-Selective Complex (CSC)". Sorting of cargo into tubules for distribution to the trans-Golgi network or the cell sur-face is achieved through the dimeric sorting nexin (SNX) component of retromer and accessory proteins such as the WASH complex which medi-ates the formation of discrete endosomal tubules enabling the sorting of cargo into distinct pathways through production of filamentous actin patch-es. In the present article, we review the molecular structure and function of the retromer and summarize the evidence linking retromer dysfunction to neurodegenerative disease.
    Language English
    Publishing date 2018-03-02
    Publishing country United Arab Emirates
    Document type Journal Article ; Review
    ZDB-ID 2033677-9
    ISSN 1875-5488 ; 1389-2029
    ISSN (online) 1875-5488
    ISSN 1389-2029
    DOI 10.2174/1389202919666171024122809
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Book ; Thesis: Staphylodermia follicularis profunda

    Reitz, Christiane

    Untersuchungen zur Therapie

    2002  

    Author's details vorgelegt von: Christiane Reitz
    Language German
    Size 96 Bl. : Ill., graph. Darst.
    Edition [Mikrofiche-Ausg.]
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Münster (Westfalen), Univ., Diss., 2002
    HBZ-ID HT013372186
    Database Catalogue ZB MED Medicine, Health

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    2002 MB 3360 order for loan Magazin

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  3. Article: Novel susceptibility loci for Alzheimer's disease.

    Reitz, Christiane

    Future neurology

    2016  Volume 10, Issue 6, Page(s) 547–558

    Abstract: Late-onset Alzheimer's disease (AD), a highly prevalent neurodegenerative disorder characterized by progressive deterioration in cognition, function and behavior terminating in incapacity and death, is a clinically and pathologically heterogeneous ... ...

    Abstract Late-onset Alzheimer's disease (AD), a highly prevalent neurodegenerative disorder characterized by progressive deterioration in cognition, function and behavior terminating in incapacity and death, is a clinically and pathologically heterogeneous disease with a substantial heritable component. During the past 5 years, the technological developments in next-generation high-throughput genome technologies have led to the identification of more than 20 novel susceptibility loci for AD, and have implicated specific pathways in the disease, in particular intracellular trafficking/endocytosis, inflammation and immune response and lipid metabolism. These observations have significantly advanced our understanding of underlying pathogenic mechanisms and potential therapeutic targets. This review article summarizes these recent advances in AD genomics and discusses the value of identified susceptibility loci for diagnosis and prognosis of AD.
    Language English
    Publishing date 2016-04-06
    Publishing country England
    Document type Journal Article
    ISSN 1479-6708
    ISSN 1479-6708
    DOI 10.2217/fnl.15.42
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: A global view of the genetic basis of Alzheimer disease.

    Reitz, Christiane / Pericak-Vance, Margaret A / Foroud, Tatiana / Mayeux, Richard

    Nature reviews. Neurology

    2023  Volume 19, Issue 5, Page(s) 261–277

    Abstract: The risk of Alzheimer disease (AD) increases with age, family history and informative genetic variants. Sadly, there is still no cure or means of prevention. As in other complex diseases, uncovering genetic causes of AD could identify underlying ... ...

    Abstract The risk of Alzheimer disease (AD) increases with age, family history and informative genetic variants. Sadly, there is still no cure or means of prevention. As in other complex diseases, uncovering genetic causes of AD could identify underlying pathological mechanisms and lead to potential treatments. Rare, autosomal dominant forms of AD occur in middle age as a result of highly penetrant genetic mutations, but the most common form of AD occurs later in life. Large-scale, genome-wide analyses indicate that 70 or more genes or loci contribute to AD. One of the major factors limiting progress is that most genetic data have been obtained from non-Hispanic white individuals in Europe and North America, preventing the development of personalized approaches to AD in individuals of other ethnicities. Fortunately, emerging genetic data from other regions - including Africa, Asia, India and South America - are now providing information on the disease from a broader range of ethnicities. Here, we summarize the current knowledge on AD genetics in populations across the world. We predominantly focus on replicated genetic discoveries but also include studies in ethnic groups where replication might not be feasible. We attempt to identify gaps that need to be addressed to achieve a complete picture of the genetic and molecular factors that drive AD in individuals across the globe.
    MeSH term(s) Middle Aged ; Humans ; Alzheimer Disease/genetics ; Genome-Wide Association Study ; Genetic Predisposition to Disease/genetics ; Mutation ; Ethnicity
    Language English
    Publishing date 2023-04-06
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2491514-2
    ISSN 1759-4766 ; 1759-4758
    ISSN (online) 1759-4766
    ISSN 1759-4758
    DOI 10.1038/s41582-023-00789-z
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  5. Article ; Online: Genetic diagnosis and prognosis of Alzheimer's disease: challenges and opportunities.

    Reitz, Christiane

    Expert review of molecular diagnostics

    2015  Volume 15, Issue 3, Page(s) 339–348

    Abstract: Alzheimer's disease (AD), the most common form of dementia in western societies, is a pathologically and clinically heterogeneous disease with a strong genetic component. The recent advances in high-throughput genome technologies allowing for the rapid ... ...

    Abstract Alzheimer's disease (AD), the most common form of dementia in western societies, is a pathologically and clinically heterogeneous disease with a strong genetic component. The recent advances in high-throughput genome technologies allowing for the rapid analysis of millions of polymorphisms in thousands of subjects has significantly advanced our understanding of the genomic underpinnings of AD susceptibility. During the last 5 years, genome-wide association and whole-exome- and whole-genome sequencing studies have mapped more than 20 disease-associated loci, providing insights into the molecular pathways involved in AD pathogenesis and hinting at potential novel therapeutic targets. This review article summarizes the challenges and opportunities of when using genomic information for the diagnosis and prognosis of AD.
    MeSH term(s) Alzheimer Disease/diagnosis ; Alzheimer Disease/epidemiology ; Alzheimer Disease/genetics ; Alzheimer Disease/therapy ; Biomarkers ; Computational Biology ; Genetic Predisposition to Disease ; Genetic Testing/methods ; Genome-Wide Association Study ; Genomics/methods ; Humans ; Prognosis
    Chemical Substances Biomarkers
    Language English
    Publishing date 2015-01-29
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2112530-2
    ISSN 1744-8352 ; 1473-7159
    ISSN (online) 1744-8352
    ISSN 1473-7159
    DOI 10.1586/14737159.2015.1002469
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  6. Article ; Online: Erratum to: The role of the retromer complex in aging-related neurodegeneration: a molecular and genomic review.

    Reitz, Christiane

    Molecular genetics and genomics : MGG

    2015  Volume 290, Issue 2, Page(s) 429

    Language English
    Publishing date 2015-04
    Publishing country Germany
    Document type Published Erratum
    ZDB-ID 2044817-X
    ISSN 1617-4623 ; 1617-4615
    ISSN (online) 1617-4623
    ISSN 1617-4615
    DOI 10.1007/s00438-015-1020-z
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  7. Article: Toward precision medicine in Alzheimer's disease.

    Reitz, Christiane

    Annals of translational medicine

    2014  Volume 4, Issue 6, Page(s) 107

    Abstract: In Western societies, Alzheimer's disease (AD) is the most common form of dementia and the sixth leading cause of death. In recent years, the concept of precision medicine, an approach for disease prevention and treatment that is personalized to an ... ...

    Abstract In Western societies, Alzheimer's disease (AD) is the most common form of dementia and the sixth leading cause of death. In recent years, the concept of precision medicine, an approach for disease prevention and treatment that is personalized to an individual's specific pattern of genetic variability, environment and lifestyle factors, has emerged. While for some diseases, in particular select cancers and a few monogenetic disorders such as cystic fibrosis, significant advances in precision medicine have been made over the past years, for most other diseases precision medicine is only in its beginning. To advance the application of precision medicine to a wider spectrum of disorders, governments around the world are starting to launch Precision Medicine Initiatives, major efforts to generate the extensive scientific knowledge needed to integrate the model of precision medicine into every day clinical practice. In this article we summarize the state of precision medicine in AD, review major obstacles in its development, and discuss its benefits in this highly prevalent, clinically and pathologically complex disease.
    Language English
    Publishing date 2014-12-14
    Publishing country China
    Document type Journal Article ; Review
    ZDB-ID 2893931-1
    ISSN 2305-5847 ; 2305-5839
    ISSN (online) 2305-5847
    ISSN 2305-5839
    DOI 10.21037/atm.2016.03.05
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  8. Article: Genetic loci associated with Alzheimer's disease.

    Reitz, Christiane

    Future neurology

    2014  Volume 9, Issue 2, Page(s) 119–122

    Abstract: The article by ... ...

    Abstract The article by Lambert
    Language English
    Publishing date 2014-11-28
    Publishing country England
    Document type Journal Article
    ISSN 1479-6708
    ISSN 1479-6708
    DOI 10.2217/fnl.14.1
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  9. Article ; Online: The role of the retromer complex in aging-related neurodegeneration: a molecular and genomic review.

    Reitz, Christiane

    Molecular genetics and genomics : MGG

    2014  Volume 290, Issue 2, Page(s) 413–427

    Abstract: The retromer coat complex is a vital component of the intracellular trafficking mechanism sorting cargo from the endosomes to the trans-Golgi network or to the cell surface. In recent years, genes encoding components of the retromer coat complex and ... ...

    Abstract The retromer coat complex is a vital component of the intracellular trafficking mechanism sorting cargo from the endosomes to the trans-Golgi network or to the cell surface. In recent years, genes encoding components of the retromer coat complex and members of the vacuolar protein sorting 10 (Vps10) family of receptors, which play pleiotropic functions in protein trafficking and intracellular/intercellular signaling in neuronal and non-neuronal cells and are primary cargos of the retromer complex, have been implicated as genetic risk factors for sporadic and autosomal dominant forms of several neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and frontotemporal lobar degeneration. In addition to their functions in protein trafficking, the members of the Vps10 receptor family (sortilin, SorL1, SorCS1, SorCS2, and SorCS3) modulate neurotrophic signaling pathways. Both sortilin and SorCS2 act as cell surface receptors to mediate acute responses to proneurotrophins. In addition, sortilin can modulate the intracellular response to brain-derived neurotrophic factor (BDNF) by direct control of BDNF levels and regulating anterograde trafficking of Trk receptors to the synapse. This review article summarizes the emerging data from this rapidly growing field of intracellular trafficking signaling in the pathogenesis of neurodegeneration.
    MeSH term(s) Aging ; Animals ; Genetic Predisposition to Disease ; Humans ; Mutation ; Neurodegenerative Diseases/metabolism ; Polymorphism, Single Nucleotide ; Protein Transport ; Receptors, Cell Surface/metabolism ; Signal Transduction ; Vesicular Transport Proteins/physiology
    Chemical Substances Receptors, Cell Surface ; Vesicular Transport Proteins
    Language English
    Publishing date 2014-10-21
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2044817-X
    ISSN 1617-4623 ; 1617-4615
    ISSN (online) 1617-4623
    ISSN 1617-4615
    DOI 10.1007/s00438-014-0939-9
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  10. Article ; Online: Dyslipidemia and the risk of Alzheimer's disease.

    Reitz, Christiane

    Current atherosclerosis reports

    2013  Volume 15, Issue 3, Page(s) 307

    Abstract: Whether cholesterol is implicated in the pathogenesis of Alzheimer's disease (AD) is still controversial. Several studies that explored the association between lipids and/or lipid-lowering treatment and AD indicate a harmful effect of dyslipidemia on AD ... ...

    Abstract Whether cholesterol is implicated in the pathogenesis of Alzheimer's disease (AD) is still controversial. Several studies that explored the association between lipids and/or lipid-lowering treatment and AD indicate a harmful effect of dyslipidemia on AD risk. The findings are supported by genetic linkage and association studies that have clearly identified several genes involved in cholesterol metabolism or transport as AD susceptibility genes, including apolipoprotein E (APOE), apolipoprotein J (APOJ, CLU), ATP-binding cassette subfamily A member 7(ABCA7), and sortilin-related receptor (SORL1). Functional cell biology studies further support a critical involvement of lipid raft cholesterol in the modulation of Aβ precursor protein processing by β-secretase and γ-secretase resulting in altered Aβ production. However, conflicting evidence comes from epidemiological studies showing no or controversial association between dyslipidemia and AD risk, randomized clinical trials observing no beneficial effect of statin therapy, and cell biology studies suggesting that there is little exchange between circulating and brain cholesterol, that increased membrane cholesterol level is protective by inhibiting loss of membrane integrity through amyloid cytotoxicity, and that cellular cholesterol inhibits colocalization of β-secretase 1 and Aβ precursor protein in nonraft membrane domains, thereby increasing generation of plasmin, an Aβ-degrading enzyme. The aim of this article is to provide a comprehensive review of the findings of epidemiological, genetic, and cell biology studies aiming to elucidate the role of cholesterol in the pathogenesis of AD.
    MeSH term(s) Alzheimer Disease/etiology ; Dyslipidemias/blood ; Dyslipidemias/complications ; Humans ; Lipid Metabolism ; Lipids/blood ; Prognosis ; Risk Factors
    Chemical Substances Lipids
    Language English
    Publishing date 2013-01-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2057369-8
    ISSN 1534-6242 ; 1523-3804
    ISSN (online) 1534-6242
    ISSN 1523-3804
    DOI 10.1007/s11883-012-0307-3
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