Remodeling Alzheimer-amyloidosis models by seeding

Abstract Alzheimer’s disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been deve...
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Autor*in:	Brittany S. Ulm [verfasserIn] David R. Borchelt [verfasserIn] Brenda D. Moore [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	Alzheimer’s disease Seeding Amyloid-β Mouse models Prion disease

Übergeordnetes Werk:	In: Molecular Neurodegeneration - BMC, 2007, 16(2021), 1, Seite 11
Übergeordnetes Werk:	volume:16 ; year:2021 ; number:1 ; pages:11

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.1186/s13024-021-00429-4

Katalog-ID:	DOAJ078084873

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spelling	10.1186/s13024-021-00429-4 doi (DE-627)DOAJ078084873 (DE-599)DOAJ82cbfc862a8b4b3ba3c24b03fd9148ea DE-627 ger DE-627 rakwb eng RC346-429 RC952-954.6 Brittany S. Ulm verfasserin aut Remodeling Alzheimer-amyloidosis models by seeding 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alzheimer’s disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been developed that replicate aspects of AD pathology. Familial AD is associated with mutations in the amyloid precursor protein and in the presenilins (associated with amyloidosis); transgenic amyloid models feature one or more of these mutant genes. Recent advances in seeding methods provide a means to alter the morphology of resultant amyloid deposits and the age that pathology develops. In this review, we discuss the variety of factors that influence the seeding of amyloid beta pathology, including the source of seed, the time interval after seeding, the nature of the transgenic host, and the preparation of the seeding inoculum. Alzheimer’s disease Seeding Amyloid-β Mouse models Prion disease Neurology. Diseases of the nervous system Geriatrics David R. Borchelt verfasserin aut Brenda D. Moore verfasserin aut In Molecular Neurodegeneration BMC, 2007 16(2021), 1, Seite 11 (DE-627)515978361 (DE-600)2244557-2 17501326 nnns volume:16 year:2021 number:1 pages:11 https://doi.org/10.1186/s13024-021-00429-4 kostenfrei https://doaj.org/article/82cbfc862a8b4b3ba3c24b03fd9148ea kostenfrei https://doi.org/10.1186/s13024-021-00429-4 kostenfrei https://doaj.org/toc/1750-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2021 1 11
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allfieldsSound	10.1186/s13024-021-00429-4 doi (DE-627)DOAJ078084873 (DE-599)DOAJ82cbfc862a8b4b3ba3c24b03fd9148ea DE-627 ger DE-627 rakwb eng RC346-429 RC952-954.6 Brittany S. Ulm verfasserin aut Remodeling Alzheimer-amyloidosis models by seeding 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract Alzheimer’s disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been developed that replicate aspects of AD pathology. Familial AD is associated with mutations in the amyloid precursor protein and in the presenilins (associated with amyloidosis); transgenic amyloid models feature one or more of these mutant genes. Recent advances in seeding methods provide a means to alter the morphology of resultant amyloid deposits and the age that pathology develops. In this review, we discuss the variety of factors that influence the seeding of amyloid beta pathology, including the source of seed, the time interval after seeding, the nature of the transgenic host, and the preparation of the seeding inoculum. Alzheimer’s disease Seeding Amyloid-β Mouse models Prion disease Neurology. Diseases of the nervous system Geriatrics David R. Borchelt verfasserin aut Brenda D. Moore verfasserin aut In Molecular Neurodegeneration BMC, 2007 16(2021), 1, Seite 11 (DE-627)515978361 (DE-600)2244557-2 17501326 nnns volume:16 year:2021 number:1 pages:11 https://doi.org/10.1186/s13024-021-00429-4 kostenfrei https://doaj.org/article/82cbfc862a8b4b3ba3c24b03fd9148ea kostenfrei https://doi.org/10.1186/s13024-021-00429-4 kostenfrei https://doaj.org/toc/1750-1326 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2009 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2055 GBV_ILN_2111 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 16 2021 1 11
language	English
source	In Molecular Neurodegeneration 16(2021), 1, Seite 11 volume:16 year:2021 number:1 pages:11
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topic_facet	Alzheimer’s disease Seeding Amyloid-β Mouse models Prion disease Neurology. Diseases of the nervous system Geriatrics
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container_title	Molecular Neurodegeneration
authorswithroles_txt_mv	Brittany S. Ulm @@aut@@ David R. Borchelt @@aut@@ Brenda D. Moore @@aut@@
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author	Brittany S. Ulm
spellingShingle	Brittany S. Ulm misc RC346-429 misc RC952-954.6 misc Alzheimer’s disease misc Seeding misc Amyloid-β misc Mouse models misc Prion disease misc Neurology. Diseases of the nervous system misc Geriatrics Remodeling Alzheimer-amyloidosis models by seeding
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topic_title	RC346-429 RC952-954.6 Remodeling Alzheimer-amyloidosis models by seeding Alzheimer’s disease Seeding Amyloid-β Mouse models Prion disease
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title	Remodeling Alzheimer-amyloidosis models by seeding
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title_sort	remodeling alzheimer-amyloidosis models by seeding
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title_auth	Remodeling Alzheimer-amyloidosis models by seeding
abstract	Abstract Alzheimer’s disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been developed that replicate aspects of AD pathology. Familial AD is associated with mutations in the amyloid precursor protein and in the presenilins (associated with amyloidosis); transgenic amyloid models feature one or more of these mutant genes. Recent advances in seeding methods provide a means to alter the morphology of resultant amyloid deposits and the age that pathology develops. In this review, we discuss the variety of factors that influence the seeding of amyloid beta pathology, including the source of seed, the time interval after seeding, the nature of the transgenic host, and the preparation of the seeding inoculum.
abstractGer	Abstract Alzheimer’s disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been developed that replicate aspects of AD pathology. Familial AD is associated with mutations in the amyloid precursor protein and in the presenilins (associated with amyloidosis); transgenic amyloid models feature one or more of these mutant genes. Recent advances in seeding methods provide a means to alter the morphology of resultant amyloid deposits and the age that pathology develops. In this review, we discuss the variety of factors that influence the seeding of amyloid beta pathology, including the source of seed, the time interval after seeding, the nature of the transgenic host, and the preparation of the seeding inoculum.
abstract_unstemmed	Abstract Alzheimer’s disease (AD) is among the most prevalent neurodegenerative diseases, with brain pathology defined by extracellular amyloid beta deposits and intracellular tau aggregates. To aid in research efforts to improve understanding of this disease, transgenic murine models have been developed that replicate aspects of AD pathology. Familial AD is associated with mutations in the amyloid precursor protein and in the presenilins (associated with amyloidosis); transgenic amyloid models feature one or more of these mutant genes. Recent advances in seeding methods provide a means to alter the morphology of resultant amyloid deposits and the age that pathology develops. In this review, we discuss the variety of factors that influence the seeding of amyloid beta pathology, including the source of seed, the time interval after seeding, the nature of the transgenic host, and the preparation of the seeding inoculum.
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title_short	Remodeling Alzheimer-amyloidosis models by seeding
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