(Q45972218)

18 December 2017

title

TGF-beta1 promotes microglial amyloid-beta clearance and reduces plaque burden in transgenic mice. (English)

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18 December 2017

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1

Wyss-Coray T

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18 December 2017

8

Mucke L

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18 December 2017

Eliezer Masliah

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object named as

Masliah E

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18 December 2017

author name string

Lin C

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18 December 2017

Yan F

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18 December 2017

Yu GQ

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18 December 2017

Rohde M

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18 December 2017

McConlogue L

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18 December 2017

language of work or name

English

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publication date

1 May 2001

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18 December 2017

published in

Nature Medicine

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18 December 2017

volume

7

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18 December 2017

page(s)

612-618

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18 December 2017

issue

5

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18 December 2017

https://scigraph.springernature.com/pub.10.1038/87945

exact match

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cites work

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Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

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Apolipoprotein E epsilon 4 allele is associated with deposition of amyloid beta-protein following head injury.

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Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition.

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Expression of human apolipoprotein E reduces amyloid-beta deposition in a mouse model of Alzheimer's disease

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Insulin-degrading enzyme regulates extracellular levels of amyloid beta-protein by degradation

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Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse

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Peripherally administered antibodies against amyloid beta-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease

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Ultrastructure of the microglia that phagocytose amyloid and the microglia that produce beta-amyloid fibrils.

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TGF-beta 1 is an organizer of responses to neurodegeneration

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Amyloidogenic role of cytokine TGF-beta1 in transgenic mice and in Alzheimer's disease

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Rodent models of Alzheimer's disease: rat A beta infusion approaches to amyloid deposits

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Transforming growth factor-betas in neurodegenerative disease

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Inflammation and Alzheimer's disease

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Chronic overproduction of transforming growth factor-beta1 by astrocytes promotes Alzheimer's disease-like microvascular degeneration in transgenic mice

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Transforming growth factor beta (TGF-?) in inflammation: A cause and a cure

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Chemotaxis by a CNS macrophage, the microglia

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Astroglial overproduction of TGF-beta 1 enhances inflammatory central nervous system disease in transgenic mice .

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Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models

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High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation

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Characterization of new polyclonal antibodies specific for 40 and 42 amino acid-long amyloid beta peptides: their use to examine the cell biology of presenilins and the immunohistochemistry of sporadic Alzheimer's disease and cerebral amyloid angiop

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7 January 2021

Amyloid precursor protein processing and A beta42 deposition in a transgenic mouse model of Alzheimer disease

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7 January 2021

Comparison of neurodegenerative pathology in transgenic mice overexpressing V717F beta-amyloid precursor protein and Alzheimer's disease

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7 January 2021

Cerebral amyloid angiopathy: amyloid beta accumulates in putative interstitial fluid drainage pathways in Alzheimer's disease

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TGF-beta in kidney fibrosis: a target for gene therapy

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Overexpression of TGF-beta 1 in the central nervous system of transgenic mice results in hydrocephalus.

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Proteoglycans and other basement membrane proteins in amyloidoses

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Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid

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Distribution of A beta-associated proteins in cerebrovascular amyloid of Alzheimer's disease.

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7 January 2021

Inflammation of the brain in Alzheimer's disease: implications for therapy.

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The apolipoprotein E epsilon 4 allele is associated with increased neuritic plaques and cerebral amyloid angiopathy in Alzheimer's disease and Lewy body variant

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7 January 2021

Identifiers

DOI

10.1038/87945

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18 December 2017

Dimensions Publication ID

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18 December 2017